HYPERTENSION A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2003 by ICON Group International, Inc. Copyright 2003 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Hypertension: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-83657-4 1. Hypertension-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on hypertension. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.
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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.
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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes & Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health
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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON HYPERTENSION ......................................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Hypertension................................................................................. 9 E-Journals: PubMed Central ....................................................................................................... 73 The National Library of Medicine: PubMed ................................................................................ 83 CHAPTER 2. NUTRITION AND HYPERTENSION ............................................................................. 175 Overview.................................................................................................................................... 175 Finding Nutrition Studies on Hypertension ............................................................................. 175 Federal Resources on Nutrition ................................................................................................. 184 Additional Web Resources ......................................................................................................... 185 CHAPTER 3. ALTERNATIVE MEDICINE AND HYPERTENSION....................................................... 191 Overview.................................................................................................................................... 191 The Combined Health Information Database............................................................................. 191 National Center for Complementary and Alternative Medicine................................................ 192 Additional Web Resources ......................................................................................................... 204 General References ..................................................................................................................... 224 CHAPTER 4. DISSERTATIONS ON HYPERTENSION......................................................................... 225 Overview.................................................................................................................................... 225 Dissertations on Hypertension .................................................................................................. 225 Keeping Current ........................................................................................................................ 236 CHAPTER 5. CLINICAL TRIALS AND HYPERTENSION ................................................................... 237 Overview.................................................................................................................................... 237 Recent Trials on Hypertension .................................................................................................. 237 Keeping Current on Clinical Trials ........................................................................................... 258 CHAPTER 6. PATENTS ON HYPERTENSION ................................................................................... 261 Overview.................................................................................................................................... 261 Patents on Hypertension............................................................................................................ 261 Patent Applications on Hypertension........................................................................................ 298 Keeping Current ........................................................................................................................ 332 CHAPTER 7. BOOKS ON HYPERTENSION ....................................................................................... 333 Overview.................................................................................................................................... 333 Book Summaries: Federal Agencies............................................................................................ 333 Book Summaries: Online Booksellers......................................................................................... 335 The National Library of Medicine Book Index ........................................................................... 362 Chapters on Hypertension ......................................................................................................... 363 Directories.................................................................................................................................. 374 CHAPTER 8. MULTIMEDIA ON HYPERTENSION ............................................................................ 377 Overview.................................................................................................................................... 377 Video Recordings ....................................................................................................................... 377 Audio Recordings....................................................................................................................... 378 Bibliography: Multimedia on Hypertension .............................................................................. 378 CHAPTER 9. PERIODICALS AND NEWS ON HYPERTENSION ......................................................... 381 Overview.................................................................................................................................... 381 News Services and Press Releases.............................................................................................. 381 Newsletters on Hypertension..................................................................................................... 384 Newsletter Articles .................................................................................................................... 386 Academic Periodicals covering Hypertension............................................................................ 387 CHAPTER 10. RESEARCHING MEDICATIONS................................................................................. 389 Overview.................................................................................................................................... 389
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U.S. Pharmacopeia..................................................................................................................... 389 Commercial Databases ............................................................................................................... 395 Researching Orphan Drugs ....................................................................................................... 396 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 401 Overview.................................................................................................................................... 401 NIH Guidelines.......................................................................................................................... 401 NIH Databases........................................................................................................................... 403 Other Commercial Databases..................................................................................................... 406 The Genome Project and Hypertension ..................................................................................... 406 APPENDIX B. PATIENT RESOURCES ............................................................................................... 411 Overview.................................................................................................................................... 411 Patient Guideline Sources.......................................................................................................... 411 Associations and Hypertension.................................................................................................. 421 Finding Associations.................................................................................................................. 427 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 429 Overview.................................................................................................................................... 429 Preparation................................................................................................................................. 429 Finding a Local Medical Library................................................................................................ 429 Medical Libraries in the U.S. and Canada ................................................................................. 429 ONLINE GLOSSARIES................................................................................................................ 435 Online Dictionary Directories ................................................................................................... 443 HYPERTENSION DICTIONARY............................................................................................... 445 INDEX .............................................................................................................................................. 573
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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with hypertension is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about hypertension, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to hypertension, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on hypertension. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to hypertension, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on hypertension. The Editors
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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON HYPERTENSION Overview In this chapter, we will show you how to locate peer-reviewed references and studies on hypertension.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and hypertension, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “hypertension” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: •
Bleeding Esophageal Varices: How to Treat This Dreaded Complication of Portal Hypertension Source: Postgraduate Medicine. 109(2): 75-76, 81-86, 89. February 2001. Contact: Available from McGraw-Hill, Inc. 1221 Avenue of the Americas, New York, NY 10020. (612) 832-7869. Summary: Bleeding esophageal varices, one of the most feared complications of portal hypertension (high blood pressure in the liver venous system), contribute to the estimated 32,000 deaths annually attributed to cirrhosis (liver scarring). This article describes the care of patients with this complication. The authors stress that successful control requires knowledge of the pertinent anatomy, underlying pathophysiology of portal hypertension, and natural history of gastroesophageal varices. The authors
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discuss the various prophylactic (preventive) and therapeutic approaches to management, including pharmacologic agents (drug therapy), endoscopic sclerotherapy, and transjugular intrahepatic portosystemic shunt (TIPS). Nonselective beta blockers are the treatment of choice for prevention of the first bleeding episode. Active bleeding is managed with octreotide and endoscopic sclerotherapy. Goals in the management of active bleeding are hemodynamic resuscitation, prevention and treatment of complications, and control of bleeding. Complications related to bleeding or its treatment can substantially increase the risk of death in each episode. TIPS and shunt surgery are reserved for those in whom octreotide and endoscopic surgery have failed. Endoscopic band ligation (tying off) should be used for prevention of recurrent bleeding. If endoscopic band ligation fails, patients can be offered TIPS or surgical therapy; they should be evaluated for liver transplantation. 4 figures. 4 tables. 11 references. •
Hypertension Management in Patients With Diabetes Source: Diabetes Care. 26(2): 355-359. February 2003. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: Clinical trials have demonstrated the importance of tight blood pressure control among patients with diabetes. However, little is known regarding the management of hypertension (high blood pressure) in patients with coexisting diabetes. This article reports on a study undertaken to determine whether hypertensive patients with coexisting diabetes are achieving lower levels of blood pressure than patients without diabetes; whether there are differences in the intensity of antihypertensive medication therapy provided to patients with and without diabetes; and whether diabetes management affects decisions to increase antihypertensive medication therapy. The authors abstracted medical records to collect detailed information on 2 years of care provided for 800 male veterans with hypertension. Of the 274 hypertensive patients with diabetes, 73 percent had a blood pressure greater than 140 over 90 mmHg, compared with 66 percent in the 526 patients without diabetes. Patients with diabetes also received significantly less intensive antihypertensive medication therapy than patients without diabetes. Less intensive blood pressure therapy in patients with diabetes could not be explained by clinicians being distracted by the treatment for diabetes. The authors conclude that there is an urgent need to improve hypertension care and blood pressure control in patients with diabetes. Additional information is required to understand why clinicians are not more aggressive in managing blood pressure when patients also have diabetes. 1 figure. 2 tables. 26 references.
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Treatment of Hypertension in Adult Patients with Diabetes Source: Diabetes Care. 25(1): 134-147. January 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: Hypertension (high blood pressure) is an extremely common comorbidity of diabetes, affecting 20 to 60 percent of people with diabetes. Hypertension is also a major risk factor for cardiovascular events, such as myocardial infarction and stroke, as well as for microvascular complications, such as retinopathy (eye disease) and nephropathy (kidney disease). This review article focuses on the treatment of hypertension in adult patients with diabetes. Recent studies have demonstrated the effectiveness of blood pressure treatment versus placebo in reducing complications of diabetes, helped to
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define the optimal level of blood pressure control, and compared treatment strategies based on different drug classes. The results of these studies support an aggressive approach to the diagnosis and treatment of hypertension in patients with diabetes in order to substantially reduce the incidence of both macrovascular and microvascular complications. Treatment decisions should be individualized based on the clinical characteristics of the patient, including comorbidities as well as tolerability, personal preference, and cost, especially for patients who must pay out of pocket for medications. Fixed dose combinations of many drugs are available and may help with compliance and be less expensive for patients with a prescription copayment. 2 tables. 117 references. •
Emergency Treatment of Upper Gastrointestinal Bleeding Due to Portal Hypertension in Cirrhotic Patients: Report on a French Consensus Meeting Source: European Journal of Gastroenterology and Hepatology. 3(5): 413-418. May 1991. Summary: In October 1989, a French national consensus meeting dealing with the emergency treatment of upper gastrointestinal bleeding of portal hypertension in cirrhosis was conducted. This article reports on that meeting, addressing the following issues: the place and the limits of digestive tract endoscopy concerning the diagnosis of bleeding source; the selection of patients in whom emergency treatment should be started; the nature of the first treatment that should be used in case of active bleeding; what measures are specific to intensive care of bleeding cirrhotic patients; how to manage upper gastrointestinal bleeding unrelated to esophageal varices in cirrhotic patients; and what to do in case of an early recurrence. 12 references.
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Cost-Effectiveness of Intensive Glycemic Control, Intensified Hypertension Control, and Serum Cholesterol Level Reduction for Type 2 Diabetes Source: JAMA. Journal of the American Medical Association. 287(19): 2542-2551. May 15, 2002. Summary: Several treatment interventions can reduce the complications associated with type 2 diabetes, but their relative cost-effectiveness is not known. This article reports on a study undertaken to estimate the incremental cost-effectiveness of intensive glycemic control (relative to conventional control), intensified hypertension (high blood pressure) control, and reduction in serum cholesterol level for patients with type 2 diabetes. Results show that the incremental cost-effectiveness ratio for intensive glycemic control is $41,384 per quality adjusted life year (QALY); this ratio increased with age at diagnosis from $9614 per QALY for patients aged 25 to 34 years to $2.1 million for patients aged 85 to 94 years. For intensified hypertension control, the cost-effectiveness ratio is minus $1959 per QALY. The cost-effectiveness ratio for reduction in serum cholesterol level is $51,889 per QALY; this ratio varied by age at diagnosis and is lowest for patients diagnosed between the ages of 45 and 84 years. The authors conclude that intensified hypertension control reduces costs and improves health outcomes relative to moderate hypertension control. Intensive glycemic control and reduction in serum cholesterol level increase costs and improve health outcomes. The cost-effectiveness ratios for these latter 2 interventions are comparable with those of several other frequently adopted health care interventions. 3 figures. 5 tables. 46 references.
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Exercise Training and the Cardiovascular Consequences of Type 2 Diabetes and Hypertension: Plausible Mechanisms for Improving Cardiovascular Health Source: JAMA. Journal of the American Medical Association. 288(13): 1622-1631. October 2, 2002. Summary: The coexistence of type 2 diabetes and hypertension (high blood pressure) is especially damaging to cardiovascular health. Most trials of exercise training for these conditions have focused on glycemic control and blood pressure reduction. Less is known about the effects of exercise on the cardiovascular consequences of diabetes and hypertension. This article reviews the available evidence and plausible mechanisms by which exercise training may improve the cardiovascular health of persons with type 2 diabetes and hypertension and provides practical guidelines for exercise prescription. A MEDLINE search was performed for January 1985 to June 2002. Bibliographies from relevant articles, professional society clinical practice guidelines, and books were also reviewed. Because few large, randomized trials exist on these topics, metanalyses, professional society clinical practice guidelines, and books were also reviewed. Type 2 diabetes and hypertension result in abnormalities in central and peripheral parameters of cardiovascular structure and function. Evidence for an exercise training benefit is strongest for improvements in endothelial vasodilator function and left ventricular diastolic function. The data for exercise training's improvement of arterial stiffness and system inflammation and for reduction of left ventricular mass are less robust. However, this assertion is based more on a lack of randomized controlled trials rather than data to the contrary. Exercise training also reduces total and abdominal fat. These changes in body composition mediate improvements in insulin sensitivity and blood pressure and may improve endothelial vasodilator function. The current evidence, albeit not fully confirmed in randomized trials, suggests that the benefits of exercise training go beyond the recognized benefits of glycemic control and blood pressure reduction. 1 figure. 1 table. 113 references.
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Portal Hypertension Source: Current Opinion in Gastroenterology. 6(3): 370-375. June 1990. Summary: The mortality rate from the initial bleeding episodes of ruptured esophageal varices is 36-70 percent, depending on the patient's hepatic reserve. This, coupled with a 1-year survival rate of 30 percent, has encouraged the identification of patients with varices that have not bled, but who are at a high risk for a bleed. This article discusses the factors that predict the first bleed, the management of varices, congestive gastropathy, and pulmonary hypertension complicating portal hypertension. The author notes that patients who seem to be at high risk for bleeding may benefit from prophylactic treatment (sclerotherapy and/or beta blockers) to prevent an impending hemorrhage. 2 tables. 33 annotated references.
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Control of Cardiovascular Risk Factors in Patients with Diabetes and Hypertension at Urban Academic Medical Centers Source: Diabetes Care. 25(4): 718-723. April 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: There are national mandates to reduce blood pressure (BP) to less than 130 over 85 mmHg, to reduce LDL cholesterol to less than 100 milligrams per deciliter, and to reduce HbA1c (glycosylated hemoglobin, a measure of blood glucose over time)
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levels to less than 7 percent, and to institute aspirin therapy in patients with diabetes. This article reports on a study undertaken to determine the proportion of patients in urban institutions with diabetes and hypertension (high blood pressure) who meet these treatment goals. Using American Diabetes Association (ADA) guidelines, the authors evaluated the control of cardiovascular disease (CVD) risk factors in 1,372 patients receiving medical care at two major urban medical centers in Brooklyn and Detroit. Information was extracted from charts of outpatient clinics. Of 1,372 active clinic patients with diabetes and hypertension, 1,247 (90.9 percent) had type 2 diabetes, and 26.7 percent met the target blood pressure. A total of 35.5 percent met the LDL cholesterol goal, 26.7 percent met the HbA1c goal, and 45.6 percent were on antiplatelet therapy (such as aspirin). Only 3.2 percent of patients met the combined ADA goal for blood pressure, cholesterol and glycosylated hemoglobin. The authors conclude that optimal control of CVD risk factors in adults with diabetes was achieved only in a minority of patients. Results reflect the inherent difficulties in achieving these complex guidelines in the present health care systems. 3 tables. 36 references. •
Hearing and Neurodevelopmental Outcome in Survivors of Persistent Pulmonary Hypertension of the Newborn Source: Pediatrics. 90(3): 392-396. September 1992. Summary: This article reports on a study that assessed neurodevelopmental outcome and hearing in infants who survived persistent pulmonary hypertension in the neonatal period, for which they were managed conservatively. A total of 27 of 34 infants with this diagnosis underwent neurological, intelligence, and audiologic testing between 10 months and 6 years of age. Children who were younger than 1 year of age at the initial hearing test were retested after they reached 2 years of age. The average IQ score was within the normal range (mean = 96.23). None of the children had sensorineural hearing loss. Severe neurologic abnormalities were seen in four children, three of whom had been severely asphyxiated at birth. Mild neurologic abnormalities were observed in five children. Two infants had bronchopulmonary dysplasia because they required supplemental oxygen for 29 and 66 days respectively, and had abnormal chest roentgenograms. The authors conclude that this study suggests that conservative management without induced alkalosis or respiratory paralysis is accompanied by no sensorineural hearing loss and a good neurologic outcome. 6 tables. 33 references. (AAM).
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Control of Hypertension in Diabetes. (editorial) Source: Diabetes Care. 26(2): 534-535. February 2003. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This editorial on the control of hypertension in diabetes serves as an introduction to an article that reports that patients with diabetes and hypertension are receiving less intensive antihypertensive therapy than patients without diabetes. In this editorial, the author discusses the reasons why this therapeutic gap in blood pressure control may exist, the difficulties of treating hypertension (high blood pressure) in patients with diabetes, the role of diabetic nephropathy (kidney disease associated with diabetes), and the role of guidelines for appropriate care of patients with diabetes and hypertension. 9 references.
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Prevention of Dementia in Randomised Double-Blind Placebo-Controlled Systolic Hypertension in Europe (Syst-Eur) Trial Source: Lancet. 352: 1347-1351. October 24, 1998. Summary: This jounral article describes the Systolic Hypertension in Europe (Syst-Eur) trial, a study exploring whether antihypertensive drug treatment could reduce the incidence of dementia. The participants in Syst-Eur had no dementia, were at least 60 years old, and had a systolic blood pressure of 160 to 219 mm Hg and diastolic below 95 mm Hg. They were treated with nitrendipine with the possible addition of enalapril, hydrochlorothiazide, or both. The data from this study showed that antihypertensive treatment was associated with a lower incidence of dementia in older people with isolated systolic hypertension. 27 references, 3 tables, 3 figures.
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Long-Term Predictors of Cognitive Outcome in a Cohort of Older People With Hypertension Source: British Journal of Psychiatry. 177: 66-71. July 2000. Summary: This journal article describes a study designed to identify early predictors of late-life cognitive outcome in a cohort of older people with mild hypertension. The study examined 387 survivors from 1,083 individuals recruited into the cognitive substudy of the Medical Research Council Treatment Trial of Hypertension in Older Adults. Researchers recorded cognitive function, premorbid IQ, and cardiovascular risk exposure on entry into the trial. This study followed up the cohort 9 to 12 years later to investigate cognitive function, update exposure status, and collect genomic material. Data analysis indicated that poorer cognitive outcome was independently related to a family history of dementia, increasing age, lower premorbid IQ, less decline in systolic blood pressure, and alcohol abstinence. The researchers concluded that reduction in systolic blood pressure among people with hypertension and moderate alcohol intake may protect against cognitive deterioration in later life. 3 tables, 30 references.
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Portal Hypertension and Variceal Bleeding Source: Current Opinion in Gastroenterology. 8: 388-397. June 1992. Summary: This review article summarizes recent advances in the area of portal hypertension and variceal bleeding. Topics include the pathophysiology of portal hypertension; Doppler ultrasound as an investigative tool in portal hypertension; the role of vasoactive drugs in treating acute variceal bleeding, including glypressin and vasopressin, somatostatin, and emergency sclerotherapy; the primary prophylaxis of variceal bleeding; prevention of rebleeding from varices; endoscopic features and portal hypertensive gastropathy; the hemodynamic effects of beta-blockers and other drugs; and noncirrhotic portal hypertension and Budd-Chiari syndrome. 76 annotated references.
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Cognitive Performance in Hypertensive and Normotensive Older Subjects Source: Hypertension. 36:1079-1082. December 2000. Summary: This study examines the association between blood pressure and cognitive function in older individuals. The study sample consisted of 107 untreated hypertensives and 116 normotensives without dementia or stroke, age 70 years or older, recruited from local general practices. Cognitive performance was measured with the Cognitive Drug Research Computerized Assessment Battery. The hypertensive group was significantly slower in all tests (simple reaction time, memory scanning, immediate
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and delayed word recognition, picture recognition, and spatial memory) except choice reaction time. In addition, accuracy was impaired in tests of number vigilence, delayed word recognition, and spatial memory. The results suggest that hypertension in older individuals may be associated with impaired cognitive function in the absence of target organ damage. 1 table, 49 references. (AA-M). •
Role of Transjugular Intrahepatic Portosystemic Shunt for Treatment of Portal Hypertension and Its Complications: A Conference Sponsored by the National Digestive Diseases Advisory Board Source: Hepatology. 22(5): 1591-1597. November 1995. Contact: Available from W.B. Saunders Company, Periodicals Department. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-3668. Summary: Transjugular intrahepatic portosystemic shunting (TIPS) is a recently developed radiological procedure that involves the creation of a parenchymal tract between the portal and hepatic veins followed by reinforcement of the tract with a metallic stent. In this article, the authors critically review the current data available on TIPS and make recommendations on the safety, efficacy, and indications for this procedure. Indications include acute variceal bleeding in which medical treatment, including sclerotherapy, has failed; recurrent variceal bleeding in patients who are refractory or intolerant to conventional medical management; treatment of refractory ascites; Budd-Chiari syndrome; and uses where TIPS is not indicated. Other topics include the contraindications to TIPS; the use of TIPS in pediatric patients; adverse effects and complications of TIPS; the efficacy and long-term patency of TIPS; research needs in this area; and recommended qualifications of physicians who perform TIPS. 78 references. (AA-M).
Federally Funded Research on Hypertension The U.S. Government supports a variety of research studies relating to hypertension. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to hypertension. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore hypertension. The following is typical of the type of information found when searching the CRISP database for hypertension:
2 Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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Project Title: A HYPERTENSION
GENE-BASED
THERAPEUTIC
FOR
PULMONARY
Principal Investigator & Institution: Brigham, Kenneth L.; Professor; Generx+, Inc. 3200 West End Ave, Ste 500 Nashville, TN 372011322 Timing: Fiscal Year 2001; Project Start 30-SEP-1998; Project End 31-OCT-2002 Summary: (Adapted from the Investigator's abstract) Primary pulmonary hypertension is a uniformly fatal disease of young and middle aged people; there is little understanding of the pathogenesis and no specific therapy. The principal pharmacologic therapy in current use is chronic constant intravenous infusion of the vasodilator prostanoid, prostacyclin. This therapy is effective, but requires maintenance of an intravenous catheter and continuous intravenous infusion; the only alternative is lung transplantation. The investigators showed some time ago that it is possible to transfect the lungs with the arachidonate cyclooxygenase (COX) gene and achieve selective increases in prostacyclin and PGE2 prostanoids which are potentially therapeutic for pulmonary hypertension. Studies supported by this phase I grant have documented that aerosol delivery of the COX gene as a plasmid-cationic liposome complex can decrease pulmonary vascular reactivity significantly in an animal model which is anatomically and physiologically similar to humans with no adverse effects on lung function. The investigators hypothesize that aerosol delivery of the COX gene in an expression plasmid complexed with cationic liposomes will prevent development and/or progression of the physiologic and pathologic changes of chronic pulmonary hypertension. The investigators further speculate that this therapy will prove superior to any current therapy for the treatment of patients with primary pulmonary hypertension and may provide a new therapeutic modality for treatment of a much larger group of patients with secondary pulmonary hypertension. In this Phase II application, the PI will determine: 1) effects of repeated administration of the COX gene in a plasmid-cationic liposome complex by aerosol on lung function, 2) prostanoid generation and pulmonary vascular reactivity in unanesthetized sheep; 3) determine whether administration of the COX gene by aerosol in a plasmid-liposome complex will prevent development or progression of sustained pulmonary hypertension and pulmonary vascular remodeling in a well-characterized chronic air embolization model of sustained pulmonary hypertension in sheep; and 4) increase the efficiency of aerosol delivery of plasmid-cationic liposome complexes by using newer generation aerosol delivery devices and improved liposome-DNA formulations. PROPOSED COMMERCIAL APPLICATION: NOT AVAILABLE Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ABNORMAL PRESSURE NATRIURESIS IN HYPERTENSION Principal Investigator & Institution: Granger, Joey P.; Professor; Physiology and Biophysics; University of Mississippi Medical Center 2500 N State St Jackson, MS 39216 Timing: Fiscal Year 2001; Project Start 01-JUL-1990; Project End 31-DEC-2004 Summary: (Verbatim from the application): A major objective of the current proposal is to examine the role of and the mechanisms whereby endothelin B receptors modulate renal-pressure natriuresis and blood pressure regulation. Endothelin- 1 acts through two receptors, ETA and ETB receptors. Both of these receptors are located in the kidney with the highest concentration of ETB receptors existing within the medulla. Although the role of ETA receptors has been well characterized in the pathophysiology of hypertension and other disease states, the physiological importance of ETB receptors in modulating renal-pressure natriuresis and blood pressure regulation is unclear.
Studies 11
Preliminary data from our laboratory indicate that the renal production of endothelin is enhanced by chronic sodium loading. Moreover, data from our laboratory and others suggest that chronic ETB receptor blockade results in a salt-sensitive form of hypertension. The exact mechanisms involved in mediating the hypertension induced by chronic ETB receptor blockade, however, are unknown. Specific aims to be addressed are: 1) To test the hypothesis that the renal endothelin system is upregulated in response to increases in sodium intake. 2) To test the hypothesis that the hypertension induced by chronic ETB receptor blockade is associated with a chronic hypertensive shift in the pressure-natriuresis relationship. 3) To test the hypothesis that the renal medulla plays an important role in mediating the hypertension induced by chronic ETB receptor blockade. 4) To test the hypothesis that reduced nitric oxide synthesis mediates the reduction in renal function and elevation in arterial pressure during ETa receptor blockade-induced hypertension. 5) To test the hypothesis that angiotensin II mediates the reduction in pressure natriuresis and elevation in arterial pressure during chronic receptor blockade-induced hypertension. 6) To test the hypothesis that ETb blockade reduces pressure-induced natriuresis by blunting the transmission of renal perfusion pressure into the renal interstitium. To test these specific hypotheses, an integrated analysis of arterial pressure, renal microcirculatory, hormonal, and sodium excretory function will be determined in a conscious, chronically-instrumented rat model of hypertension induced by chronic ET1 receptor blockade. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: AC-SDKP IN TARGET ORGAN DAMAGE IN HYPERTENSION Principal Investigator & Institution: Carretero, Oscar A.; Division Head; Case Western Reserve Univ-Henry Ford Hsc Research Administraion Cfp-046 Detroit, MI 48202 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant) Hypertension is a cardiovascular risk factor that often leads to target organ damage. Angiotensin-converting enzyme inhibitors (ACEi) significantly reduce cardiovascular events, especially in high-risk patients. The effects of ACEi are mediated by inhibition of both the conversion of Ang I to Ang II and kinin degradation. We have evidence that in hypertension another peptide hydrolyzed by ACE, N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), prevents and reverses cardiac fibrosis without altering blood pressure (BP) or cardiocyte hypertrophy. This is the first demonstration that administration of Ac-SDKP has an effect on cardiac fibrosis; however, we do not know whether Ac-SDKP has a physiological role, the mechanism by which it inhibits fibrosis or whether it contributes to the cardiovascular protective effects of ACEi. In this project we propose to test the general hypothesis that in hypertension cardiac fibrosis is the result of an alteration of the balance between pro-fibrotic and proinflammatory vs anti-fibrotic and anti-inflammatory systems. Ac-SDKP alters this balance in favor of the latter, reversing fibrosis (an important component of target organ damage) and improving cardiac function. The mechanisms by which Ac-SDKP antagonizes pro-fibrotic stimuli are: a) directly by inhibiting fibroblast proliferation and collagen synthesis and b) indirectly by acting as an anti-inflammatory cytokine, thus inhibiting production of TGF beta 1 and other cytokines and macrophage activation and infiltration. We also hypothesize that part of the anti-fibrotic effect of ACEi on target organ damage is mediated by Ac-SDKP interacting synergistically with kinins and NO. To test this hypothesis, we propose to conduct in vivo studies, using a combination of physiological, pharmacological and molecular approaches (gene deletion). In the first two aims we will determine the mechanisms by which Ac-SDKP prevents and reverses cardiac fibrosis. In Aim 1 we will study its effect on fibroblast proliferation and collagen
12 Hypertension
synthesis and degradation. In Aim 2 we will study whether Ac-SDKP inhibits cardiac fibrosis in part by acting as an anti-inflammatory cytokine, decreasing proinflammatory cytokines and macrophage activation and infiltration and reactive oxygen species production. In Aim 3, we will study whether in hypertension Ac- SDKP improves diastolic dysfunction by reversing cardiac fibrosis. In Aim 4 we will determine whether endogenous Ac-SDKP antagonizes the inflammatory and fibrotic effect of angiotensin II (Ang II), aldosterone, and myocardial infarction (MI). In addition, we will study whether part of the cardiovascular protective effect of ACEi is due to an increase in AcSDKP, which interacts with kinins and NO to decrease extracellular matrix deposition in the cardiovascular system. These studies are significant since they will demonstrate: 1) the mechanism by which Ac-SDKP decreases cardiac fibrosis; 2) whether it has a therapeutic effect, improving diastolic and systolic dysfunction by reversing cardiac fibrosis; 3) whether it has a physiological role by antagonizing pro-fibrotic stimuli in the cardiovascular system; and 4) whether it mediates the cardiovascular protective effect of ACEi. In the future, non-peptidic analogues of Ac-SDKP could be developed to treat fibrosis in hypertension, aging, heart failure (HF) post-MI, diabetes and other diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ADAPTATIONS TO HYPOXIA Principal Investigator & Institution: Mcmurtry, Ivan F.; Professor; Medicine; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2001; Project Start 01-APR-1977; Project End 31-MAR-2003 Summary: This is a resubmission seeking renewal of a 25-year program encompassing 4 sub-projects. The present application sharpens the focus of the laboratory on the pulmonary circulation, by a multi-faceted study of the mechanisms of hypoxic pulmonary circulation, by a multi-faceted study of the mechanisms of hypoxic pulmonary hypertension (PH). The work is collectively founded on the hypothesis that PH smooth muscle cell (SMC) function. Studies of functional contributions explore the influence of hypoxia on the ratio of pulmonary vasoconstrictors/dilators and of altered ion channel function . Work exploring structural aspects tests the idea that there exist specific subpopulations of hypoxia-responsive SMCs responsible for a preponderance of remodeling of lung vessels in hypoxia and that hypoxic proliferative response is dependent on specific isoforms of protein kinase C. The projects share experimental models of hypoxic pulmonary hypertension in rats and cows, as well as 3 core laboratories. This project will test 3 specific aims: 1) If hypoxic pulmonary hypertension is associated with increased endothelial NOS but not ET-1 protein, whereas the opposite is true in genetic pulmonary hypertension; 2) If the mechanisms of action of nitric oxide synthase (eNOS) and ET-1 gene expression are hypoxia and hemodynamic stress, respectively in these models. This project will investigate 4 specific aims: 1) What changes in PA SMC ion channels develops as a result of hypoxic pulmonary hypertension; 2) How does Ca2+ enter the hypertensive PA SMC; 3) How do NO and cGMP regulate ion channels in the hypertensive PA SMC; and 4) Are changes in ion channel expression and regulation a direct result of chronic hypoxia. This project will test 3 hypothesis: 1) Gi coupled receptors activate the MAPK signaling pathway in selected populations of PA SMCs; 2) Hypoxia selectively stimulates in hypoxiaresponsive PA SMCs through MAPK-dependent mechanisms; and 3) Connective Tissue Growth Factor (CTGF), is expressed selectively in subpopulations of PA SMCs during hypoxia and contributes to the fibroproliferative response. This project will test 2 specific aims: 1) Are PKC-alpha expression and activation critical determinants of PA
Studies 13
SMC proliferation to hypoxia in vivo, and 2) Are PKC-alpha expression and activation critical determinants of PA SMC proliferation to hypoxia in vitro. The 4 projects are highly interactive both conceptually, as well as in the performance and communication of experimental results. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ADRENERGIC RECEPTORS AND HYPERTENSION IN BLACKS Principal Investigator & Institution: Lockette, Warren E.; Professor; Internal Medicine; Wayne State University 656 W. Kirby Detroit, MI 48202 Timing: Fiscal Year 2001; Project Start 01-MAY-1995; Project End 31-MAY-2002 Summary: (Verbatim from the application): Abnormalities in sympathetic nervous system activity have been reported for many patients with salt-sensitive, essential hypertension. Autonomic responsiveness is mediated by alpha-2 adrenergic receptors (A2ARs). During the previous funding cycle, we performed an extensive populationbased association study. We reported that a common mutation of the A2AR was associated with severe hypertension in Detroit Blacks. This polymorphism was also associated with increased platelet aggregation, altered baroreceptor sensitivity, and diminished salt excretion in healthy, college-age students with no evidence of high blood pressure. We postulated that severe blood pressure elevations may be a "marker" of individuals at risk for stroke due to a common gene defect encoding increased vascular resistance and platelet sensitivity. In this continuation, we will measure the proportion of the total variance of A2AR-mediated platelet aggregation and central baroreceptor activity that may be attributable to additive genetic factors in humans. A2AR-mediated platelet aggregation will be measured with standard laboratory techniques. Autonomic responses to increases and decreases in baroreceptor activity will be assessed by loading, and unloading, of the central blood volume with immersion in thermal-neutral water and graded lower body negative pressure (LBNP), respectively. We postulate that abnormal A2AR-mediated transport of chloride is a necessary link between the autonomic nervous system and salt-sensitive hypertension. Before that hypothesis can be proven, we must first establish the mechanism(s) by which A2AR agonists affect chloride transport. We documented a role for A2ARs in mediating intracellular chloride transport. We will now use microfluorometry to test our hypothesis that A2AR-dependent agonists mediate increases in intracellular chloride concentrations ([Cl-]i) in platelets and vascular smooth muscle by enhancing the activity of the chloride/bicarbonate exchanger and the Na/Cl and the Na/K/2Cl-coupled cotransporters in these effector cells. We predict: (1) a significant heritable component exists for platelet aggregation, heart rate responses to LBNP, and immersion-induced salt excretion; (2) the squared difference of measurements for a particular phenotype between sibs negatively correlate with the number of alleles shared at the C10 A2AR locus; and (3) agonist-induced increases in platelet calcium and aggregation are enhanced by A2AR-dependent increases in {Cl-]i mediated by the chloride/bicarbonate exchanger. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ANGIOTENSIN, HYPERTENSION
SODIUM
AND
GENES
IN
PRIMATE
Principal Investigator & Institution: Shade, Robert E.; Southwest Foundation for Biomedical Res San Antonio, TX 782450549 Timing: Fiscal Year 2003; Project Start 01-APR-2002; Project End 31-MAR-2006
14 Hypertension
Summary: (provided by applicant): Sodium-dependent hypertension has long been associated with a defect in renal function. Experimental models as well as human studies have also suggested that an alteration in genetic expression may contribute to the hypertensive process. Sodium-lithium countertransport (SLC) activity is one mechanism that helps maintain intracellular sodium concentrations, and in some hypertensive patients, SLC activity is increased. These individuals also experience an inappropriate response to sodium challenges that appears to result from a lack of suppression of the renin-angiotensin-aldosterone system (RAAS). The association between SLC activity and hypertension is genetically determined since it occurs in families. It is uncertain whether this reflects an alteration in the gene for SLC, one of the genes that may increase RAAS function, or an interaction between genes for the two systems. The goal of the proposed studies is to examine the relationship between SLC activity and the RAAS in a non-human primate model in which the SLC phenotype is high or low. The hypothesis to be tested is that a high SLC activity is associated with inappropriately high RAAS function and a greater arterial pressure sensitivity to dietary sodium. In three aims, the contributions of peripheral and central RAAS components to sodium-dependent hypertension will be studied in baboons with the high and low SLC phenotypes. In the first aim, regulation of the RAAS will be examined in high and low SLC animals during a step-wise increase in sodium intake. These experiments will determine whether animals with high SLC activity have a reduced ability to suppress the RAAS and develop salt-sensitive hypertension. The second aim will investigate the role of angiotensin and aldosterone in the stimulation of hypertension by sodium and their ability to cause blood pressure to rise in high and low SLC animals. This aim will determine whether by raising plasma angiotensin or aldosterone the high SLC animals are more likely to become hypertensive. The third aim will focus on central nervous system mechanisms associated with an inappropriately high RAAS in high and low SLC animals. These studies will determine whether the high SLC activity results in more sensitive central mechanisms driving the sympathetic nervous system to raise arterial pressure. These studies will help provide data to determine whether an inappropriately high RAAS activity can cause hypertension. Importantly, this work will also reveal whether the genetically determined phenotype of high SLC is important in predisposing an animal to sodium-dependent hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ARTERIAL HYPERTENSION
BARORECEPTOR
UNLOADING
CAUSES
Principal Investigator & Institution: Thrasher, Terry N.; Surgery; University of Maryland Balt Prof School Baltimore, MD 21201 Timing: Fiscal Year 2002; Project Start 01-JAN-2002; Project End 31-DEC-2005 Summary: (provided by the applicant): This application is based on the hypothesis that unloading arterial baroreceptors can cause hypertension. We have developed a model with carotid baroreceptors on one side functional (all other carotid and aortic baroreceptors denervated) in conscious dogs. In this model, ligation of the common carotid artery proximal to the innervated carotid sinus produces a significant and sustained increase in systemic arterial pressure (SAP, 22 +/- 3 mmHg for at least seven days duration, n=6) and plasma renin activity (PRA). Carotid ligation unloads baroreceptors downstream and the reflex increase in SAP returns mean carotid sinus pressure (CSP) to control levels. The cause of the increase in SAP must be related to unloading carotid baroreceptors because removing the ligature on the innervated side after seven days results in a reduction in SAP to control levels. Furthermore, ligation of
Studies 15
the common carotid on the denervated side results in a fall in CSP distal to the ligature and does not cause an increase in SAP (n=4). The goal of this application is to elucidate the mechanisms, which drive the hypertension in this model. The aims are first, to extend the observations to include continuous measurements of SAP with the animals in their home cages using telemetry. The second aim is to test the hypothesis that the renal nerves are essential for the maintenance of the hypertension. Carotid baroreceptors will be unloaded as above in dogs with denervated kidneys. The third aim will test the hypothesis that the hypertension is primarily due to an increase in peripheral resistance by measuring cardiac output and pressure simultaneously. The fourth aim will test the hypothesis that increased sympathetic efferent activity is responsible for the hypertension. Control experiments will utilize ligation of the carotid proximal to a denervated carotid sinus. The health implications of this project are startling because current theories disregard participation of baroreceptors in the long-term control of blood pressure. These studies will provide a new framework for understanding the development and maintenance of hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ARTERIAL COMPRESSION OF THE VENTRO-LATERAL MEDULLA Principal Investigator & Institution: Patel, Sunil J.; Neurological Surgery; Medical University of South Carolina 171 Ashley Ave Charleston, SC 29425 Timing: Fiscal Year 2002; Project Start 05-APR-2002; Project End 31-MAR-2007 Summary: (provided by applicant) The Principal Investigator (PI) is a full time academic neurosurgeon who specializes in surgery of the posterior fossa for neurovascular compression syndromes. This research career award will afford him the time to acquire the skills needed to perform further patient-oriented research in neurogenic hypertension and obtain a Master of Science degree in Clinical Research. The research and training experience he will obtain during the period of the K23 Award will allow him to become an independent clinical investigator with a focus on mechanisms of neurogenic hypertension, and to be able to design and conduct studies on its therapy. The PI has the commitment and support of his sponsor, department and institution to permit the time and allocate the resources needed to attain his research career goals and complete his proposed research. Training will be facilitated through the institutions K30 Award and a NIH supported GCRC. The hypothesis to be tested is that neurogenically mediated hypertension is caused by arterial compression of areas along the retroolivary sulcus of the ventro-lateral medulla. Therefore the aims of the project are to: 1) electrically establish in humans the locations along the normal surface of the ventrolateral medulla that are sensitive to stimulation and produce pressor responses; and 2) show an association between arterial compression of these 'pressor-sensitive' areas along the medullary surface (established in Aim 1) and aberrations in sympathetic tone and cardiovascular functions in volunteering subjects with neurogenic hypertension. Hemodynamic and sympathetic response patterns to electrical stimulation of the medullary surface will be recorded to map the location of the pressor-regulating neuronal groups under the surface of the ventro-lateral medulla in patients undergoing surgery of the posterior fossa. This information on response patterns will then be used in a second study to investigate associations between arterial compression of these pressor-regulating areas and similar measured patterns in hypertensive individuals. Results from this research should help to better define the physiologic criteria to be used to relate arterial compression of the ventro-lateral medulla to neurogenic hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
16 Hypertension
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Project Title: AT2 RECEPTOR MECHANISMS IN ANG II DEPENDENT HYPERTENSION Principal Investigator & Institution: Carey, Robert M.; Professor and Dean; Medicine; University of Virginia Charlottesville Box 400195 Charlottesville, VA 22904 Timing: Fiscal Year 2001; Project Start 01-MAY-1998; Project End 31-MAR-2003 Summary: The overall objective is to test the hypothesis that the angiotensin II (ANG II) subtype-2 (AT2) receptor plays an important counter-regulatory role in the control of blood pressure in ANG II-dependent hypertension through the renal generation of vasodilator substances. The specific aims will test two hypotheses in ANG II-dependent hypertension: (1) that the AT2 receptor mediates enhanced renal production of bradykinin (BK) and/or nitric oxide (NO) and (2) that AT1 and AT2 receptors regulate renal prostaglandin E2 (PGE2), both leading to counter-regulatory renal vasodilation. The investigators have developed a rat model of renovascular hypertension, the 2kidney, 1-wrap (Grollman) hypertensive rat and have demonstrated that the hypertension is ANG II-dependent. In this model, the investigators have demonstrated that AT2 receptor blockade prevents the hypotensive response to AT1 receptor blockade, indicating that the AT2 receptor mediates counter-regulatory vasodilation. Using a novel renal interstitial fluid (RIF) microdialysis technique, the investigators have demonstrated in the normal rat that the AT2 receptor mediates ANG II induced renal NO production. The proposed experiments represent a systematic approach to the role of the AT2 receptor in the renal production of BK, NO and PGE2 and their roles in renal vasodilation in ANG II-dependent hypertension. RIF levels of these mediators will be determined in response to AT2 receptor blockade, and distal pathways will be dissected to determine the mechanisms by which AT2 receptors mediate counterregulatory changes. The proposed studies will provide for the first time in any form of hypertension an understanding of the relevance and mediators of AT2 receptors in the long term control of blood pressure and kidney function. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BIOLOGY OF MONOCROTALINE INDUCED PULMONARY HYPERTENSION Principal Investigator & Institution: Segall, Henry J.; Vet Molecular Biosciences; University of California Davis Sponsored Programs, 118 Everson Hall Davis, CA 95616 Timing: Fiscal Year 2002; Project Start 01-JAN-1993; Project End 31-MAR-2006 Summary: Monocrotaline (MCT) induced pulmonary hypertension remains a principle model for the biology and development of intervention strategies for the human disease. Current concepts of pulmonary hypertension (PH) assign a primary pathogenetic role to the pulmonary endothelial cell in both human PH and that induced by MCT. Recently, a genetic lesion in the Bone Morphogenic Protein Receptor (BMPR) has been identified in humans with pulmonary hypertension The overall objective of this grant is to characterize the effects of MCT on the biology of the pulmonary endothelial cell and relate them to the initiating mechanisms of PH. Our previous work has demonstrated that several proteins with potential functional significance for endothelial cells have selective covalent interactions with the reactive intermediate of MCT metabolism, monocrotaline pyrrole (MCTP). This leads to our hypothesis that protein targets of MCT initiate vascular remodeling by altering endothelial cell function similar to endothelial dysfunction in persons with genetic susceptibility to primary pulmonary hypertension. Our specific aims are to further characterize the protein targets of MCT, to determine the functional significance of protein binding in endothelial cells, to evaluate proteins
Studies 17
regulating endothelial cell barrier function as potential MCT targets and to determine whether the MCT model alters the BMPR signal pathway affected in humans with PH. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BLOOD FLOW, CONTRACTILE AND METABOLIC FUNCTION IN LVH Principal Investigator & Institution: Davila-Roman, Victor G.; Associate Professor of Medicine, Anesthe; Internal Medicine; Washington University Lindell and Skinker Blvd St. Louis, MO 63130 Timing: Fiscal Year 2001; Project Start 01-APR-1998; Project End 31-MAR-2003 Summary: Hypertension, a disease that affects more than 50 million Americans, is the most common cause of left ventricular hypertrophy (LVH). Over 20 percent of patients with hypertension have LVH, and its presence is associated with a 50 percent increase in cardiovascular morbidity, and a risk of mortality from cardiovascular disease that is four to six times greater than the risk from hypertension alone. Because of this, regression of LVH with antihypertensive medication has become a goal of treatment. The precise mechanisms by which cardiac hypertrophy in arterial hypertension increases cardiac morbidity and mortality remain unknown. Although it is known that structural abnormalities of the myocardium and the microcirculation in LVH result in decreased coronary flow reserve, the relation between these and abnormalities in contractile, and metabolic function are unknown. It is also unkown whether regression of LVH induced by pharmacologic intervention decreases the risk of subsequent cardiovascular disease. Hence, understanding the mechanisms responsible for the transition from hypertrophy to heart failure, and elucidating whether reversal of LVH with antihypertensive medication results in salutary effects to the coronary circulation and cardiac function and whether it is associated with reduced morbidity and mortality from cardiovascular disease is of great importance. The working hypotheses of this proposal are: a) that hypertensive LVH is associated with decreased coronary artery reserve, and that this is associated with abnormalities in metabolic and contractile function; and b) that pharmacologic therapy with ACE inhibitors result in normalization of the left ventricular mass and improvements in myocardial blood flow reserve, myocardial metabolism, and systolic function. We propose to prove these hypotheses by use of novel approaches and methods, most of which have been developed and validated at our institution. These methods include imaging techniques that allow measurements of left ventricular mass with echocardiography, myocardial blood flow by positron emission tomography (PET) with 15 O- water, global contractile function with magnetic resonance imaging (MRI) with and without tissue-tagging by stressstrain relations, and myocardial metabolism measured by PET with 11 C-acetate and 11 C- palmitate. Measurements at baseline and after one year of treatment with ACE inhibitors will be performed in patients with LVH induced by hypertension and with either normal or decreased left ventricular function. Results of these studies are designed to determine the benefits of normalization of arterial blood pressure and left ventricular mass with antihypertensive medication. We have previously used and validated these methods and preliminary studies from our institution suggests that the cardiac imaging approach outlined in this proposal is rational and feasible. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BOLD MRI: APPLICATION TO INTRARENAL OXYGENATION Principal Investigator & Institution: Prasad, Pottumarthi V.; Evanston Northwestern Healthcare 2650 Ridge Ave Evanston, IL 60201
18 Hypertension
Timing: Fiscal Year 2003; Project Start 01-FEB-1998; Project End 31-JAN-2008 Summary: (provided by applicant): Hypertension, also known as high blood pressure, affects one in four adults in the United States, and is a major risk factor for stroke, heart attack and kidney disease. It is sometimes called the "silent killer" because it often has no symptoms. Progress towards preventing and curing hypertension has been impeded by a lack of thorough understanding of its underlying pathophysiology. Significant progress made over the last decade in vascular biology has allowed for better understanding of many of the underlying mechanisms, which then has led to development of novel drug treatments for hypertension. Many now believe that kidney plays an important role in the pathophysiology of hypertension. Specifically, it is thought that renal medullary blood flow has a direct influence on hypertension. It is still a topic of debate as to the alterations in the kidney being the cause or the consequence of hypertension. In either case, availability of a non-invasive method to probe blood flow at a regional level within the kidney would allow for verifying many of the hypotheses to be tested in humans. Based on previous experience with blood oxygenation level dependent (BOLD) magnetic resonance imaging (MRI) technique to the kidney, we hypothesize that the technique would be sensitive to changes in medullary blood flow. More specifically, we believe that the technique in combination with suitable endothelium-dependent vasoactive agents would allow for renal microvascular reactivity studies to be performed in a non-invasive way. Vascular reactivity studies look for responses in the vessel walls to vasoactive substances or physiological paradigms that elicit an endogenous vasoactive response. It is believed that these functional changes at the microvascular level take place much earlier than the development of hypertension and if detected early enough, may be reversed with novel therapeutic approaches. In this proposal, we will perform experiments that will validate our hypothesis in several forms of hypertension in previously well established animal models and then extend them to human kidneys. Animal models will allow for direct comparison of BOLD MRI measurements against invasive laser probe assessments. Our human studies are designed to test the hypothesis that subjects at risk for developing hypertension will exhibit reduced renal microvascular reactivity. Successful outcome will provide better understanding of pathophysiology of human hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BRAIN AND CARDIAC ANGIOTENSIN II IN HYPERTENSION Principal Investigator & Institution: Berecek, Kathleen H.; Professor; Physiology and Biophysics; University of Alabama at Birmingham Uab Station Birmingham, AL 35294 Timing: Fiscal Year 2001; Project Start 01-DEC-1983; Project End 31-MAR-2004 Summary: The major goal is to identify mechanisms underlying the prolonged antihypertensive and cardio-protective effects of early, short- term ACE inhibitor therapy or single intracardiac injection of the angiotensin II AT1 receptor subtype antisense cDNA (AT1 R-AS) to SHR. This goal is based on previous studies by us and other investigators showing that early, short-term therapy with captopril (CAP) or early, single-application of AT1 R-AS to SHR attenuated hypertension not only in treated rats but in their offspring as well. The major hypothesis to be tested is that Ang II is a permissive factor necessary for expression of the hypertensive phenotype and that early perturbation of this peptide, particularly in brain or heart, either by decreasing its synthesis and/or effecting its receptors would prevent expression of hypertension in treated rats as well as their offspring. There are four Specific Aims to this project. Aim I: To determine whether or not the prolonged antihypertensive effect of early, short-term CAP therapy in SHR is due to chronically attenuated production of Ang II and/or its
Studies 19
receptors which is passed on to offspring of treated rats and/or due to accumulation of antihypertensive agents such as bradykinin (BK), Ang (1-7) or nitric oxide (NO) which are passed on to offspring of treated rats. Aim II: To determine whether or not the prolonged antihypertensive effect of early CAP treatment down-regulates the AT1 receptor subtype (AT1 R) in brain and, with it, produces an attenuation of Ang II mediated modulation of the sympathetic nervous system. Aim III: To determine whether the prolonged antihypertensive effect of early CAP treatment down-regulates AT1 R in heart and, with it, produces an attenuation of Ang II mediated effects on cardiovascular structural remodeling. Aim IV: To determine whether or not early AT1 R antisense therapy in SHR mimics changes in brain and cardiac receptors and their function observed with early, short-term CAP therapy. We will perform histological, morphological, biochemical, molecular biological and functional studies to address there hypotheses. The proposal addresses an important cardiovascular problem, that of the role of brain and cardiac renin-angiotensin systems in the development of hypertension and its sequelae and why early perturbation of these systems with early, short-term ACE therapy or a single early application of AT1 R-AS leads to a permenant effect not only in the development of hypertension in SHR subjected to these treatments but also in their offspring. These studies are highly novel and could help to define new strategies not only for the treamtent of hypertension but its prevention as well. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CARDIOVASCULAR REGULATION--AUTONOMIC/METABOLIC MECHANISMS Principal Investigator & Institution: Biaggioni, Italo; Professor of Medicine and Pharmacology; Vanderbilt University 3319 West End Ave. Nashville, TN 372036917 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2007 Summary: (provided by applicant): Local metabolic factors play an important role in modulating vascular smooth muscle tone, and interact with the autonomic nervous system to contribute to cardiovascular regulation. Nitric oxide (NO) is arguably one of the most important of these metabolic factors. Experimental evidence suggests that endothelial-derived NO exerts tonic vasodilatory effects even under resting conditions. Neuronal-derived NO acts centrally to inhibit sympathetic tone, and on presynaptic aderenergic neurons to inhibit norepinephrine release. There is substantial evidence that several disease states are characterized by ?NO deficiency?, including hypercholesterolemia, smoking and, potentially, hypertension. It is though that this NO deficiency contributes to the adverse cardiovascular events that characterizes these patient populations. Experimental systemic blockade of NO synthesis leads to an increase in blood pressure, indicating its importance on cardiovascular regulation. In normal subjects, however, the pressor effect of systemic NO inhibition is modest because of the restraining effect of the baroreflex. It is difficult, therefore, to gauge the importance of NO on blood pressure regulation because of the 'close loop' characteristics of autonomic regulation. Similarly, the relative contribution of neuronal NO and endothelial NO to blood pressure control remains unclear. It would be advantageous, therefore, to develop a human model where the increase in blood pressure produced by systemic NOS inhibition reflects selective endothelial NO inhibition, unrestrained by baroreflex buffering. Patients with pure autonomic failure represent such a human model. Similarly, we can induce transient autonomic failure by blocking neurotransmission at the level of autonomic ganglia with trimethaphan. We propose to use these models to test the hypothesis that endothelial nitric oxide is an important modulator of blood pressure under normal conditions, and that its impairment
20 Hypertension
contributes to hypertension. We will inhibit NO synthesis with L-arginine analogs to determine its effect on normal subjects, normotensive offspring of hypertensive parents, patients with essential hypertension, and patients with pure autonomic failure. About half of patients with pure autonomic failure paradoxically develop hypertension driven by increased vascular resistance. We also propose a proof-of-concept study to determine if modulation of NO mechanisms with L-citrulline and Larginine provide a novel therapeutic option in this human model of hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CEREBROVASCULAR HYPERTENSION
CHANGES
IN
PREGNANCY
AND
Principal Investigator & Institution: Cipolla, Marilyn J.; Neurology; University of Vermont & St Agric College 340 Waterman Building Burlington, VT 05405 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): Eclampsia is a serious complication of pregnancy that occurs when hypertension develops with neurologic symptoms, including headaches, nausea, visual disturbances and convulsions. While numerous organs are affected by hypertension in pregnancy, cerebrovascular involvement is the direct cause of death in approximately 40 percent of patients. The major cerebrovascular changes that occur have been shown to be similar to hypertensive encephalopathy in which acute elevations in blood pressure (i.e., acute hypertension) overcome the myogenic vasoconstriction of the cerebral arteries and arterioles causing autoregulatory failure, hyperperfusion and edema. Because women who develop eclampsia in general are normotensive prior to pregnancy, there is evidence that pregnancy affects the cerebral circulation in a way that makes the vessels susceptible to autoregulatory failure and hyperperfusion during acute hypertension. The long-term objective of this proposal is to investigate how pregnancy affects the structure and function of the cerebral circulation focusing on diameter regulation in response to changes in pressure (myogenic reactivity) and how those changes affect vascular permeability that promotes edema. Aim 1 will use isolated and pressurized posterior cerebral arteries from pregnant and nonpregnant rats to determine the pressure at which forced dilatation occurs and investigate underlying mechanisms of pregnancy-induced alterations in diameter regulation, including vascular smooth muscle actin and endothelial cell influences (e.g., nitric oxide and prostaglandins). In addition, since hypertension alone has been shown to cause significant remodeling and reactivity changes in the cerebral circulation, Aim 1 will also investigate how elevated mean arterial pressure during pregnancy affects myogenic activity and diameter regulation in a rat model of hypertension in pregnancy (nitric oxide inhibition). Acute hypertension and eclampsia are associated with significant edema formation due to disruption of the normally impermeable cerebral endothelium. Therefore, Aim 2 will investigate pregnancyinduced changes in endothelial cell permeability during acute hypertension, including enhanced fluid phase endocytosis (transcellular flux) and tight junction disruption (paracellular flux). The influence of pregnancy on permeability during forced dilatation will be determined using a combination of techniques, including clearance of fluorescent tracers and transmission electron microscopy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CIRCUMVENTRICULAR ORGANS: GENDER AND HYPERTENSION Principal Investigator & Institution: Hay, Meredith; Director and Associate Professor; None; University of Missouri Columbia 310 Jesse Hall Columbia, MO 65211
Studies 21
Timing: Fiscal Year 2001; Project Start 15-FEB-2000; Project End 31-JAN-2004 Summary: It has been proposed that estrogen delays and or prevents the onset of hypertension and may function to keep women "cardiovascularly younger" than men of the same age. Similar observations have been made in experimental hypertensive animals, however, the underlying mechanisms of estrogen's protective effects are incompletely understood. Given the importance of estrogen replacement therapy in women's health, it is clear that an understanding of the cellular mechanisms underlying estrogen's cardiovascular protective effects is critical for continuing development of clinical therapies for the treatment of hypertension in women. Angiotensin II (Ang II) is an important factor in some forms of both clinical and experimental hypertension. Chronic intravenous infusions of low levels of Ang II in experimental animals result in an increase in blood pressure that involves an increased neurogenic contribution to the maintenance of blood pressure which is prevented by prior lesioning of the area postrema (3,6,33,57,95). It is thought that circulating Ang II acts on area postrema neurons to maintain the hypertension. The proposed studies will test the general hypothesis that estrogen protects against the Ang II induced hypertension by inhibiting the actions of Ang II on area postrema neurons. To test this hypothesis and to characterize the effects of estrogen (17beta-estradiol) on area postrema neurons, Ang II induced increases in blood pressure and baroreflex modulation, this proposal will utilize whole-cell patch clamp recordings from isolated area postrema neurons, in vivo single unit recordings of area postrema neurons and hemodynamic measurements in conscious animals to address the following 4 major and distinct aims. 1) To evaluate area postrema membrane properties following exposure to 17beta-estradiol. 2) To determine the effects of acute and chronic 17beta-estradiol on area postrema calcium handling. 3) To determine the effect of 17beta-estradiol on activation of area postrema neurons. 4) To evaluate the effects of acute and chronic 17beta-estradiol on Ang II hypertension. Determination of the effects of estrogen on CNS mechanisms underlying Ang II dependent hypertension will have a significant impact on our understanding of the cardiovascular benefits of estrogen replacement therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EFFECTS HYPERTENSION
OF
BMPRII
MUTATIONS
IN
PULMONARY
Principal Investigator & Institution: Rodman, David M.; Professor; Medicine; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2003; Project Start 19-SEP-2003; Project End 31-JUL-2007 Summary: (provided by applicant): Primary pulmonary hypertension (PPH) is a potentially lethal disorder characterized by pulmonary vasoconstriction and vascular remodeling involving abnormal proliferation of fibroblasts, smooth muscle and endothelial cells. In the year 2000, mutations in the type 2 bone morphogenic protein receptor (BMPR2) were identified as the genetic basis for familial PPH and about 30% of sporadic PPH. BMP signaling had not previously been connected to pulmonary hypertension, and the mechanistic linkage is unknown. We hypothesize that in normal individuals the BMP pathway acts to down-regulate both inflammatory cytokinemediated positive feedback loops and vascular smooth muscle cell proliferation. Insufficient BMP pathway activity in individuals with BMPR2 mutations leads to insufficient damping of these auto-regulatory loops, resulting in the PPH phenotype. We provide preliminary evidence in cell culture systems supporting this hypothesis and have constructed a unique series of transgenic mice to further test the hypothesis. These
22 Hypertension
mice express a human dominant-negative BMPR2 (dnBMPR2) using the tetracycline gene switch system, allowing both spatial and temporal control of expression. We have successfully bred smooth muscle cell and epithelial cell specific dnBMPR2 expressing mice, and are constructing endothelial cell specific mice at this time. Using our in vitro and transgenic models we will test the following three specific aims: 1: Test the hypothesis that the BMP pathway is a negative modulator of the cytokine interleukin-6 (IL-6) in PA SMC, leading to reduced IL-6-mediated signaling and proliferation. 2: Test the hypothesis that loss of PA SMC BMPR2 function in SM22-dnBMPR2 transgenic mice leads to an exaggerated pulmonary hypertensive response in vivo. 3: Test the hypothesis that loss of BMPR2 function in lung cell types other than SMC also contributes to the development of pulmonary hypertension. Upon completion of our studies, we will have tested the hypothesis that the link between BMP signaling and pulmonary hypertension involves both regulation of the critical cytokine, IL-6, as well as modulation of smooth muscle cell proliferation. We will have also tested the role of four pulmonary cell types, smooth muscle, endothelium, airway epithelium and macrophages in the link between BMPR2 and pulmonary hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CONTROL
ENDOGENOUS
OPIOIDS,
PAIN
AND
BLOOD
PRESSURE
Principal Investigator & Institution: Mccubbin, James A.; Professor and Chair; Psychology; Clemson University 300 Brackett Hall Clemson, SC 296345702 Timing: Fiscal Year 2001; Project Start 01-AUG-1989; Project End 31-JUL-2003 Summary: This proposal is for continuation of our ongoing research on opioid abnormalities and blood pressure reactivity in persons at risk for hypertension. We are gradually becoming aware that regulation of both blood pressure and pain sensitivity is altered in pre-hypertensive populations. For example, persons at risk for hypertension have decreased opioid inhibition of blood pressure responses to stress. Paradoxically, they also show antinociceptive effects consistent with exaggerated opioid function. The scientific meaningfulness, both basic and clinical, of the links between pain sensitivity alterations and blood pressure dysregulation remains to be clarified. Recent studies by ourselves and others have emphasized the importance of opioids in regulation of 1) neuroendocrine and blood pressure responses to stress in hypertension development, 2) behavioral responses to pain, and 3) the relationship between pain sensitivity and blood pressure. The purpose of this continuation proposal is to further examine the role of endogenous opioids in blood pressure dysregulation by studies of circulatory and behavioral responses to aversive stimuli in persons at enhanced risk for hypertension. This will be accomplished by comparison of the effects of opioid blockade with naltrexone on pain sensitivity and blood pressure reactivity in young men and women with mildly elevated casual blood pressure. We hypothesize that abnormalities of both blood pressure control and pain sensitivity in the early stages of hypertension development are linked to altered opioid peptide function. Persons at risk for hypertension will show exaggerated opioid inhibition of pain sensitivity in the face of diminished opioid inhibition of blood pressure reactivity. Improved understanding of the opioidergic basis of altered pain sensitivity and blood pressure control will clarify the poorly characterized etiology of essential hypertension and possibly offer new preventive, diagnostic and therapeutic strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
Studies 23
•
Project Title: ESOPHAGEAL VARICES BY B-ADRENERGIC BLOCKERS Principal Investigator & Institution: Groszmann, Roberto J.; Internal Medicine; Yale University 47 College Street, Suite 203 New Haven, CT 065208047 Timing: Fiscal Year 2001; Project Start 20-APR-1993; Project End 31-MAR-2003 Summary: Cirrhosis is the fifth leading cause of death in the United States in individuals under the age of 65, the productive years of life. It affects men and women equally, and impacts on all races and socio- economical levels. Portal hypertension is the main complication of cirrhosis, regardless of etiology. Gastroesophageal varices and variceal hemorrhage are a direct consequence of portal hypertension and account in large part for the high mortality of cirrhosis. Non-selective beta- adrenergic blockers decrease portal pressure and have been shown to prevent the first variceal hemorrhage in patients with cirrhosis and varices. Early portal hypotensive therapy, before the patients develop varices, would be beneficial not only because it may prevent or delay the formation of varices (and variceal hemorrhage) but because it may prevent or delay the development of other complications of portal hypertension, such a ascites. This ongoing multi-center, prospective, randomized, placebo-controlled, double-blind trial was designed with the primary aim of investigating if early therapy with timolol, a nonselective beta-adrenergic blocker, can prevent or delay the development of varices in patients with cirrhosis and portal hypertension. Secondary aims will examine whether timolol prevents or delays other complications of portal hypertension such as ascites and porto-systemic encephalopathy, as well as liver transplantation or death. Patients with cirrhosis, without varices on endoscopy and with portal hypertension (portal pressure greater than 6 mmHg) are included in the study. This grant application was funded in April of 1993 and patient randomization began in August of 1993. Patient accrual took longer than originally estimated, however it is now certain that the number of 190 patients required for the study will have been randomized by the end of the current funding period (March 1998), since at the writing of this proposal 158 patients had already been randomized. In calculating sample size, we assumed a rate of development of varices of 50 percent at 4 years in the control arm, to be reduced to 30 percent in the timolol arm. So far our observed rates for development of varices are consistent with our planned estimates. However, we have now estimated that a minimum follow-up of 4 years (after last patient is recruited) is necessary to ensure high statistical power (80 percent at the 2-sided 0.05 level). The trial is highly significant for the promise it holds for the treatment of cirrhosis of all etiologies and for an understanding of the natural history of the disease. The four centers involved are widely renown for their studies in this area and have collaborated productively in the past, including the only published double-blind trial of propranolol in the prevention of first variceal hemorrhage in patients with cirrhosis and varices. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ESTROGEN AND SODIUM MODULATE HYPERTENSION IN AGING RATS Principal Investigator & Institution: Hinojosa-Laborde, Carmen; Associate Professor; Physiology; University of Texas Hlth Sci Ctr San Ant 7703 Floyd Curl Dr San Antonio, TX 78229 Timing: Fiscal Year 2002; Project Start 01-FEB-2002; Project End 31-JAN-2007 Summary: (provided by applicant): The Dahl salt sensitive (S) rat will be studied as an animal model of post-menopausal hypertension to investigate the mechanisms responsible for the hypertension. The pressor systems that will be evaluated are the
24 Hypertension
renin-angiotensin system (RAS) and the sympathetic nervous system (SNS). The role of estrogen, aging, and salt intake as modulators of these pressor systems via their effects on the nitric oxide (NO) system will be investigated. The first specific hypothesis is that the aging process with the accompanying loss of estrogen activity is associated with a down regulation of the nitric oxide system resulting in hypertension. To test this hypothesis, Specific Aim 1 of this study is to monitor blood pressure and the level of activation of the NO system in intact, ovariectomized (OVX), and OVX+estrogen-treated Dahl salt sensitive and Dahl salt-resistant (R) female rats as they age from 3 month to 2022 months of age. The second specific hypothesis is that the factors maintaining the hypertension associated with the loss of estrogen activity in Dahl S rats is determined by the level of salt intake. OVX performed at young, middle and old age will cause an increase in blood pressure, but the rise will be attenuated with increasing age. However, the level of blood pressure and the activity of the pressor systems contributing to hypertension will be higher pre-OVX because of the effects of aging on the RAS and SNS. Two specific aims will address this hypothesis. Specific Aim 2 will be to establish that the Dahl S elderly and OVX females maintained on low salt intake will become hypertensive as a result of an activation of the RAS. Estrogen administration will maintain activation of the NO system to suppress the RAS. Blockade of NO formation in low salt animals will increase RAS function, especially in the OVX+estrogen animals. Specific Aim 3 is to determine that high salt fed Dahl S elderly and OVX animals will develop a hypertension that is dependent on the activation of the SNS. As with the low salt animals, estrogen supplement will suppress the SNS stimulation through a NOmediated mechanism. Together these studies will provide evidence that the arterial pressure of the Dahl S rat is sensitive to the removal of estrogen through OVX or aging suggesting a useful model of post-menopausal hypertension. By investigating the relationship of estrogen, NO and salt, important new information will be gained in the mechanisms whereby estrogen provides protection against hypertension. Importantly, a greater understanding will be obtained addressing why the protection disappears with the aging process. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ESTROGEN REDUCES VENOUS TONE IN EARLY HYPERTENSION Principal Investigator & Institution: Martin, Douglas S.; Basic Biomedical Sciences; University of South Dakota 414 E Clark St Vermillion, SD 57069 Timing: Fiscal Year 2001; Project Start 15-SEP-2000; Project End 31-JUL-2004 Summary: (Verbatim from the application): Recent data from our laboratory indicated that venous tone is increased in the developmental stages of spontaneous hypertension in the rat. Since the increase in blood pressure in the initial stages of hypertension is characterized by an elevation of cardiac output, veins appear to play an important role in the initiation of the hypertensive process. The development of hypertension is sexually dimorphic. Considerable evidence suggests that estrogen attenuates the development of hypertension. Estrogen has been shown to affect vascular smooth muscle via both endothelial dependent and independent mechanisms and to modulate peripheral and central nervous system function. Veins possess functional estrogen receptors, high estrogen states are associated with changes in venous tone and estrogen modulates neural activity in brain regions involved in the control of venous tone. Thus, estrogen may modulate venoconstrictor tone during the developmental stages of hypertension via effects on venous smooth muscle and/or via effects on sympathetic outflow to veins. Accordingly, the proposed research is aimed at testing the general hypothesis that estrogen reduces venoconstrictor tone during the developmental stages
Studies 25
of spontaneous hypertension. The specific aims of the research will be to determine if I) Estrogen reduces sympathetic venoconstrictor tone in young female SHR. II) Estrogen reduces venous tone via effects on venous smooth muscle responsiveness via an effect on the nitric oxide system, calcium channels or potassium channels. III) Estrogen alters the expression of key proteins involved in the control of venous tone. Experiments will be performed in spontaneously hypertensive (SHR) rats at 6-10 weeks of age, a time point when previous studies have shown elevated venous tone in SHR rats. MAP, HR, and mean circulatory filling pressure, an index of integrated venomotor tone will be measured in conscious rats to determine the effects of estrogen on overall venous tone. Isolated portal and mesenteric veins will be used to assess the effects of estrogen on venous smooth muscle responsiveness and the mechanisms underlying these effects. Western blot techniques will be used to determine if estrogen affects venous tone by altering expression of key protein involved in venous control systems. These studies are expected to show that estrogen attenuates the development of hypertension by reducing venomotor tone and thereby, reduces a major factor contributing to the increase in cardiac output and blood pressure that initiates the hypertensive process. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ETIOLOGY OF NEPHROPATHY AND HYPERTENSION IN AASK PATIENT Principal Investigator & Institution: Lipkowitz, Michael S.; Medicine; Mount Sinai School of Medicine of Nyu of New York University New York, NY 10029 Timing: Fiscal Year 2001; Project Start 01-AUG-2000; Project End 31-JUL-2005 Summary: (adapted from the application) We will study the etiology of hypertension and nephropathy in the majority of the 1094 African-American patients in the AfricanAmerican Study of Kidney Disease in Hypertension (AASK). The AASK study is an NIH sponsored clinical multicenter trial comparing the effect of two levels of blood pressure control and three antihypertensive regimens on progression of hypertensive nephropathy in African Americans. There is a disproportionate number of African Americans with hypertensive target organ damage, suggesting a genetic susceptibility in this population; paradoxically, few studies have been performed to evaluate such genetic predisposition to disease in this high risk population. The patients of the AASK study offer a unique opportunity to prospectively determine the genetic factors involved in hypertension and hypertensive target organ damage within a high risk and understudied population. The proposed studies will immortalize white blood cells from patients to provide a renewable source of tissue and DNA from this unique study group, and follow two approaches in assessing the etiology of hypertension, nephropathy, and their sequelae: 1. Studies are proposed to determine whether polymorphisms in candidate genes for hypertension, renal failure, and cardiac disease, including renin-angiotensin system genes, insulin resistance (beta3-adrenergic receptor and lipoprotein lipase) genes, Liddle's syndrome (beta and gammaENaC) genes, and others are related to hypertension or renal failure, severity/rate of progression of renal disease, severity/refractoriness of hypertension, electrocardiographic left ventricular hypertrophy, cardiovascular morbidity and mortality, and overall morbidity and mortality. 2. Additional studies will employ a new technique, mapping by admixture linkage disequilibrium (MALD), which uses the linkage disequilibrium caused by recent admixture of founder populations to localize genes linked to a particular phenotype within a 5-20 centiMorgan region in a genome-wide screen. By utilizing microsatellite markers from the carefully phenotyped patients of the AASK Study it should be
26 Hypertension
possible to identify regions of interest containing genes associated with hypertension, renal failure, and the outcomes described above for candidate genes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FEEDBACK CONTROL BY H3 RECEPTORS IN HYPERTENSIVE Principal Investigator & Institution: Washington, Benny; Tennessee State University 3500 Centennial Blvd Nashville, TN 37203 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2006 Summary: H3 histamine receptors provide feedback inhibition of synthesis and release of histamine from the hypothalamus, as well as, inhibition of the release of other neurotransmitters, such as acetylcholine from intestinal cholinergic nerves, and norepinephrine from the retina and cerebral cortex. Preliminary data indicate that the ability of H3 receptors to regulate feedback inhibition of histamine release in spontaneously hypertension rats is age-dependent. Our central hypothesis is sustained hypertension enhances H3-receptor's ability to regulate the synthesis and release of histamine in the CNS. To test this hypothesis we will: 1) assess changes in the evokedrelease of histamine in the CNS (hypothalamus); 2) investigate quantitatively, changes in H3-histaminergic receptors in the CNS (hypothalamus); and 3) identify changes in the expression of H3 receptor mRNAs in the CNS (hypothalamus) using RT-PCR during the progression of hypertension. The proposed studies will be conducted in the CNS of spontaneously hypertensive (SHR) phenotypes and compared with normotensive (WKY) rats-accepted models for essential hypertension during the progession of hypertension. The results/data obtained will define the role of histamine in the development of hypertension and the function of the H3 receptor in upregulation or downregulation of histamine. The information generated from this investigation will also provide important insights into the pathophysiological causes of hypertension and could offer an opportunity to develop potential new drugs for the management of hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: FETAL ORIGINS OF ADULT HYPERTENSION IN MICROSWINE Principal Investigator & Institution: Bagby, Susan P.; Professor of Medicine; Oregon Health & Science University Portland, OR 972393098 Timing: Fiscal Year 2002; Project Start 01-JUN-2002; Project End 31-MAY-2007 Summary: A growing body of human epidemiologic evidence links intrauterine growth retardation (IUGR) and adult "Syndrome X": hypertension, obesity, diabetes, coronary artherosclerosis, and risk of renal failure. In preliminary studies in microswine, maternal isocaloric protein restriction (0.5% vs. 14%) during nephrogenesis (last 1/3 gestation +3 weeks post- natally) yields IUGR at 3 weeks, rapid catch-up growth to 123% of control body weight (overweight), adult hypertension, reduced nephron number by histology, and normal GFR suggesting single-nephron hyperfiltration. Renal cortical AT1 and AT2 receptors by quantitative autoradiography are abnormal in both 3-week and 6-month old offspring of low-protein sows but in unique ways. We hypothesize that excess appetite/body image size generate excess protein load for the low number of nephrons, driving sustained intrarenal renin/AngII (RAS) activation to achieve nitrogen balance via single-nephron hyperfiltration. This RAS response is predicted to amplify the Na retention and extracellular fluid volume (ECV) excess expected with fewer nephrons, yielding hypertension. In a microswine model of maternal protein restriction/IUGR, studies in offspring will address: 1) whether IUGR modifies the activation state of
Studies 27
circulating vs. intrarenal RAS at key developmental stages (preterm; 2-weeks postnatal; 3-month pre- hypertensive juvenile; and 6-month adult), including mRNA, protein, and activity levels for renin, angiotensinogen, ACE, AngII, and AT1/AT2 receptors at LowProtein vs. Normal-protein offspring on ad lib normal diet; 2) whether IUGR enhances postnatal homeostatic responses of blood pressure (BP), ECV, Na balance, and circulating vs. intrarenal RAS components in vivo to dietary sodium manipulation to AngII blockade; 3) whether IUGR amplifies AT1 signaling efficacy in vitro in cultured vascular smooth muscle at each developmental stage; and 4) whether global caloric restriction to limit adult bodyweight to 75% of Normal-protein controls in IUGR offspring attenuates adult BP, body fat mass, ECV, and intrarenal RAS components. Results are relevant to etiologic mechanisms of hypertension and to the preventive management of IUGR-exposed children at risk for adult cardiovascular and renal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GAMMA-MSH AND SODIUM METABOLISM Principal Investigator & Institution: Humphreys, Michael H.; Professor; Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, CA 94122 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): Variations in dietary sodium intake initiate integrated adjustments in neural and hormonal systems regulating sodium excretion by the kidneys in order to maintain overall sodium balance. These adjustments remain incompletely understood despite intensive study. In addition, a complex relationship exists between sodium balance and blood pressure such that high dietary sodium intake provokes hypertension in susceptible individuals. Studies from our laboratory have identified a previously unrecognized hormonal system which participates in the maintenance of sodium balance on a high sodium intake. This system involves the synthesis of the prohormone proopiomelanocortin (POMC) in the pituitary, and its processing into the secreted natriuretic peptide gamma-melanocyte stimulating hormone (gamma-MSH). This system is activated by a high sodium diet in rats, mice, and humans, and fails to respond to sodium loading in rodents with genetic forms of hypertension. We shall characterize the hypertension seen with dietary sodium loading in mice with gamma-MSH deficiency due to targeted disruption of the proconvertase 2 gene, necessary for processing of POMC into gamma-MSH, and establish that the hypertension is corrected by infusion of gamma-MSH. We shall also evaluate the consequences of inhibition of gamma-MSH release from the pituitary by dopaminergic stimulation in rats fed a high sodium diet, and test the effects of sodium loading in mice lacking melanocortin receptors with which gamma-MSH interacts. In addition, we shall characterize the nature and location of renal melanocortin receptors, and determine if their expression is altered by a high sodium diet. We shall determine if gamma-MSH acts centrally to inhibit sympathetic nervous outflow and lower blood pressure in hypertensive PC2 -/- mice on the high sodium diet. Finally, we shall examine the effects of high vs low sodium diets on blood pressure and plasma gamma-MSH concentration in normal subjects and patients with mild essential hypertension studied in a General Clinical Research Center to determine if this system functions in humans in a manner parallel to that in rodents and evaluate if individuals with salt-sensitive hypertension demonstrate blunted activation of the system. These studies should extend our understanding of the integrated regulation of sodium balance when challenged with a high sodium intake, and the relationship between sodium intake and the development
28 Hypertension
of hypertension, by providing mechanistic insight into a novel and previously unrecognized system activated by high dietary sodium intake. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENES OF HYPERTENSION IN AFRICAN AMERICANS Principal Investigator & Institution: Kotchen, Theodore A.; Professor of Medicine; Medicine; Medical College of Wisconsin Po Box26509 Milwaukee, WI 532264801 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2007 Summary: (provided by applicant): We hypothesize that we will be able to identify genes contributing to hypertension in African Americans by focusing on the physiological pathways that determine arterial pressure. Over the past 6 years, we have extensively characterized African Americans for phenotypes related to cardiovascular and renal function. Based on recently completed genome scans, we have identified several chromosomal regions likely to contain genes influencing hypertension-related phenotypes in hypertensive, African American sib pairs. For several phenotypes, overlapping QTLs have also been identified in related studies in a genetically isolated French Canadian population and/or in homologous chromosomal regions in the F2 cross of Dahl-salt sensitive x normotensive Brown Norway rats. We now propose to extensively phenotype 500 hypertensive and 500 normotensive African American subjects to conduct a genetic association study, using a SNP genomic scan approach. To achieve a clear separation of blood pressures from hypertensive subjects, normotensive subjects will be selected from the lower third of the population-based blood pressure distribution. Hypertensive (BMI), and age. Inclusion of phenotypes is based on their relevance to the pathophysiology of hypertension and prior evidence of "heritability." Candidate genes for SNP analysis will be selected within chromosomal regions of two QTLs that we have previously demonstrated to be linked to hypertension-related phenotypes--a QTL for body mass index on chromosome 1 and a QTL for microalbuminuria on chromosome 18. SNP analyses will be carried out in 15 percent of the genes within each of these QTLs, and genes will be selected on the basis of their relevance to hypertension, including documented sequence conservation for blood pressure related QTLs with rat or mouse. The final goal of the project is to determine if distinct clusters of blood pressure related phenotypes can be identified that will permit stratification of hypertensive individuals into distinct subgroups to facilitate the analysis of the genetic determinants of hypertension and/or provide mechanistic leads to genes contributing to these traits. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETIC DETERMINANTS OF HYPERTENSION, LVH, AND CHF Principal Investigator & Institution: Dries, Daniel L.; Internal Medicine; University of Texas Sw Med Ctr/Dallas Dallas, TX 753909105 Timing: Fiscal Year 2002; Project Start 17-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): The endogenous cardiac hormonal system (CHS) moderates blood pressure, the development of left-ventricular hypertrophy (LVH) in response to hypertension, and delays progression of systolic heart failure. The "afferentlimb" of the CHS refers to the ability of the myocardium to release atrial and brain natriuretic peptide (ANP and BNP) in response to pressure overload, and the "efferentlimb" describes the biological action of these hormones in target tissue. Plasma levels of cGMP are tightly correlated with the efferent actions of the cardiac hormones providing a validated method to measure the efferent function of the CHS in humans. We
Studies 29
hypothesize that gene-environment interactions involving genes related to critical components of the afferent and efferent cardiac hormonal signaling pathways, and gene-gene interactions between these genotypes and the ACE-gene, contribute to interindividual variation in susceptibility to hypertensive heart disease. Moreover, differences in the frequencies of these alleles in special populations may explain the increased susceptibility of African-Americans to LVH, development of heart failure, and progression of established heart failure. In order to address these hypotheses, we will identify patients with untreated hypertension and LVH in a random population sample of approx. 3,000 subjects. We will then compare the afferent and efferent function of the CHS in African- American and Caucasian subjects with untreated hypertension and leftventricular hypertrophy, and identify phenotypes characterized by reduced function of either the afferent or efferent function of the CHS. We will sequence these subjects to identify sequence variants in candidate genes critical to the cardiac hormonal signaling pathways (the gene for ANP, BNP, the type A and C cardiac hormone receptors, and corin). We will then study the association of these genotypes with prevalent hypertension, cardiac MRIdetermined LVH, and prevalent hypertensive cardiomyopathy in the two ethnic cohorts. In addition we will analyze the association of these genotypes with prognosis in patients with advanced systolic heart failure. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETIC EXPRESSION OF RISK GENES IN HYPERTENSION Principal Investigator & Institution: Seely, Ellen W.; Professor; Brigham and Women's Hospital 75 Francis Street Boston, MA 02115 Timing: Fiscal Year 2001; Project Start 25-JUN-2001; Project End 31-MAY-2005 Summary: (Verbatim from the application): Hypertension is a major contributor to cardiovascular disease, the leading cause of death in US women. Most studies of hypertension have focused on men. Women have a lower incidence of hypertension until age 50 at which time, the incidence of hypertension in women becomes greater than that in men. Since age 50 is the average age of menopause in US women, this observation suggests that ovarian steroids, present in the premenopausal state, mask genetic predisposition to hypertension and that with loss of these steroids at menopause, genetic predisposition to hypertension becomes manifest. We have shown that a specific intermediate phenotype of essential hypertension is associated with polymorphisms of the angiotensinogen gene which result in greater tissue activity of the renin-angiotensin-aldosterone system (RAAS) as a possible cause of hypertension. This phenotype is uncommon in premenopausal women compared to age-matched men but the frequency of this phenotype increases at menopause becoming equal in men and women. Estradiol has major effects on many of the genes of the RAAS and therefore is a prime candidate for modulating the expression of genotype and being responsible for the change in phenotype frequency in pre versus postmenopausal women. The overall objectives of this proposal are to: 1) demonstrate a difference in frequency of specific polymorphisms of genes of the RAAS in premenopausal hypertensive women as compare to hypertensive postmenopausal women and men, 2) test the hypothesis that the administration of estradiol to postmenopausal hypertensive women with these specific polymorphisms in RAAS genes will alter the intermediate phenotype and lower blood pressure, 3) examine activity of the tissue RAAS according to specific genotypes in these three groups. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
30 Hypertension
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Project Title: GENETIC LINKAGES IN CALCIUM OXALATE STONE DISEASE Principal Investigator & Institution: Mandel, Neil S.; Professor; Medicine; Medical College of Wisconsin Po Box26509 Milwaukee, WI 532264801 Timing: Fiscal Year 2003; Project Start 15-AUG-2003; Project End 31-MAY-2008 Summary: (provided by applicant): Kidney stone disease is a substantial health problem associated with significant pain, suffering, and economic costs. 5% to 15% of the population will have a symptomatic episode of a stone by the age of 70 and at least 50% of these individuals will have recurrent disease. To date, the only well-defined genetic abnormalities leading to hyperoxaluria and calcium oxalate stone disease have been described for primary and secondary hyperoxaluria and associated with specific enzyme errors. However, the familial tendency of idiopathic calcium oxalate stone disease coupled with the common trend for stone recurrence have led to the speculation that many idiopathic calcium oxalate stone formers may have a genetic predisposition for their stone disease. We propose to explore the genetic linkages underlying idiopathic hyperoxaluria and calcium oxalate stone disease, utilizing and applying to stone disease the methods and genetic observations from existing animal models currently being used to explore the genetic basis of hypertension. The application of genomic methods to stone disease is new. The proposed studies will allow us to define the genetic linkages that mediate critical mechanistic events in idiopathic calcium oxalate stone disease including the initiation, progression, and physiologic consequences of hyperoxaluria, crystalluria, and calcium oxalate crystal retention. We will use available genomic rat resources to explore both the genetic linkages in calcium oxalate stone disease and the genetic linkages between calcium oxalate stone disease and hypertension. Three specific major breeding colonies will be used: 1) The Dahl SS rat that demonstrates salt sensitive hypertension, 2) A colony of Brown Norway rats that are about 62% consomic with the Dahl SS rat, and 3) Consomic strains of Dahl SS rats that have one chromosome at a time introgressed into the Dahl SS genetic background from the Brown Norway rat, creating a rat that is about 98% consomic with the parent Dahl rat. Our working hypothesis is that there are specific genetic linkages that are associated with idiopathic hyperoxaluria and calcium oxalate stone disease and that the pathophysiology of stone disease associated with hypertension is different from stone disease absent hypertension. There are three Specific Aims. Specific Aim I: To determine what the associative effect of hypertension and hyperoxaluria is on urine chemistry and how these associated challenges influence the potential for calcium oxalate stone disease. Specific Aim II: To define the specific tissue injury associated with hypertensive and with hyperoxaluric challenges and to correlate these findings with effective calcium oxalate crystal attachment and stone maturation. Specific Aim III: To identify the chromosomes that harbor genes that control major susceptibility and resistance to hyperoxaluria, calcium oxalate crystalluria, and stone disease using a chromosomal replacement panel of consomic Dahl SS rats. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETIC STUDIES OF MINERALOCORTICOID FUNCTION Principal Investigator & Institution: Geller, David S.; Internal Medicine; Yale University 47 College Street, Suite 203 New Haven, CT 065208047 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-JAN-2005 Summary: (adapted from the application) Hypertension is one of the most common diseases in America--being present in a 20% of the population. It is also one of the leading causes of morbidity and mortality in the United States, via its effects on heart,
Studies 31
cerebrovascular and renal disease. Despite its prevalence, the underlying cause(s) of hypertension remain poorly understood. It is clear that there are environmental and hereditary genetic factors that predispose to the development of hypertension; identification of the genetic factors is made difficult, however, by the small effects of many genes coupled with overlying environmental factors. One approach to this problem has been to study single gene disorders that primarily affect blood pressure. The determinants of the molecular bases of glucocorticoid-remediable aldosteronism, Liddle's syndrome, Bartter's syndrome, Gitelman's syndrome and others has done to [sic] much to increase our understanding of renal physiology and the kidneys role in blood pressure regulation. In this project, we describe the discovery of a new form of mendelian hypertension caused by activating mutation in the mineralocorticoid receptor, the effector molecule for aldosterone in the distal nephron. Through characterization of the affected kindred and in vitro analysis of the mutant receptor, we will discern the mechanism by which the mutation activates mineralocorticoid receptor function. It is anticipated that this information will yield insight into normal receptor function, which may prove useful in drug design. By creating a mouse model of the disease, we hope to generate a mechanism to study the effects of a wide variety of steroid agonists and antagonists in vivo, and also to gain insight into the effects of the activated mineralocorticoid receptor in tissues other than the kidney. This project is designed to provide training in molecular and human genetics for the Principal Investigator and to enable him to develop a career in academic Nephrology with a focus on the molecular genetics of hypertension and renal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETIC STUDY ENDOTHELIAL FUNCTION (PILOT)
OF
ARTERIAL
COMPLIANCE
AND
Principal Investigator & Institution: Li, Rongling; Morehouse School of Medicine Atlanta, GA 30310 Timing: Fiscal Year 2002; Project Start 30-SEP-1987; Project End 31-JUL-2006 Summary: (provided by applicant): The objective of this pilot study is to develop and implement standardized methods for investigating both genetic and environmental determinants of endothelial function and arterial compliance (elasticity) in African Americans. African Americans have stiffer arteries and a higher prevalence of hypertension compared to other ethnic groups in the US. Specific genetic makeup and environmental factors may work together to influence the susceptibility. The specific aims of this pilot study are: 1) to develop standardized methods for collecting and validating family data from African-American hypertensive and normotensive probands, their family members and first-degree relatives; 2) to assess the difference in allele and genotype frequency, endothelial function, vascular compliance and blood pressure within and between the two sets of families; 3) to compare the distribution of genetic, behavioral, physical, psychosocial, biochemical and other environmental risk factors in families with or without high family risk of hypertension; and 4) to estimate preliminarily genetic and environmental determinants to familial clustering of risk factors, endothelial dysfunction, arterial stiffness and hypertension. The study will use family-based case-control design. We propose to recruit 5 African- American families in which probands (40% females) and at least one of their parents have hypertension, and 5 African-American families with probands (40% females) and both parents to be free of hypertension. Married individuals aged 30-50, who have both parents alive and at least two children and two siblings, will be included as probands in this study. An interviewer-administered questionnaire will be utilized to obtain information on
32 Hypertension
participants. demographic, behaviors, lifestyles, medical history, and family history of cardiovascular disease, socioeconomic status and other cardiovascular risk factors. Participants will have physical examinations, and measurements of arterial compliance and brachial endothelial function. Blood samples will be obtained to determine genotypes of endothelial nitric oxide synthase (eNOS) and angiotensin-converting enzyme (ACE), blood chemistry, hematology and lipid profiles, and to establish cell lines for future genetic studies of arterial disease. Statistical analyses will be conducted to estimate the main effects of genetic and environmental risks for arterial stiffness and their interactions among gene-gene and gene-environmental factors, such as smoking or physical inactivity, controlling for other cardiovascular risk factors. This study has the potential to provide insights into strategies for recruiting multi-generational families within the African-American community and the etiology and pathogenesis of arterial disease which will allow the development of effective strategies for early prevention of arterial disease, and its sequelae in an under-studied and under- served population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETICS OF SALT SENSITIVITY IN AFRICAN AMERICANS Principal Investigator & Institution: Douglas, Janice G.; Professor; Medicine; Case Western Reserve University 10900 Euclid Ave Cleveland, OH 44106 Timing: Fiscal Year 2001; Project Start 15-MAY-2000; Project End 31-MAR-2005 Summary: The prevalence, morbidity, and mortality of arterial hypertension are disproportionately high in the African-American population. Essential hypertension is a polygenic and heterogeneous disorder. In particular, African-Americans display an amplified blood pressure response to salt. The cellular and molecular mechanisms of salt-sensitive hypertension in humans remain poorly defined and our knowledge of potential genetic mechanisms remains incomplete. We recently observed an augmented blood pressure response to a salt challenge in healthy non-obese African- Americans females as compared to Whites. African-Americans also had significantly higher intracellular Na and depressed activity of the Na pump (86 Rb uptake)as compared to Whites suggesting these may be important phenotypic markers of salt-sensitive hypertension. In fact, an increase in intracellular Na was positively correlated with the increases in systolic blood pressure following one week of low salt vs one week of high salt diet in African-Americans but not in Whites. The inverse relationship was noted for the Na pump in African-Americans. The proposed study will carry out genetic studies of sibships with at least two hypertensive embers ascertained from the AfricanAmerican population. Emphasizing model- free approaches to genetic linkage analysis based upon hypertensive sibling pairs, candidate genes that have been associated with salt-sensitive hypertension in either human or animal studies will be evaluated with respect to these intermediate phenotypes, and blood pressure responses to a salt challenge. The aims of this proposal are: l) To characterize the intermediate phenotypes of salt sensitivity, intracellular Na, sodium pump activity, and protein expression in a cohort of 500 hypertensive siblings in 160 sibships and to genotype these individuals; wherever possible, parents of these subjects will also be genotyped in order to better establish identity by descent relationships. 2) To assess linkage of the various candidate loci with intermediate phenotypes relating to the magnitude of blood pressure change with a salt challenge using univariate and multivariate approaches. The overall aim of this project is to improve our understanding of the genetic basis and phenotypic characterization of salt-sensitive hypertension in African Americans. To this end, careful analytic attention will be paid to the development of improved phenotype
Studies 33
definition, as well as to the consideration of gene-gene and gene-environment interaction. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETICS OF VASCULAR REMODELING IN HYPERTENSION Principal Investigator & Institution: Berk, Bradford C.; Professor & Chairman; Medicine; University of Rochester Orpa - Rc Box 270140 Rochester, NY 14627 Timing: Fiscal Year 2001; Project Start 01-JUN-1999; Project End 31-MAY-2003 Summary: An important long-term goal in the approach to treating atherosclerosis and hypertension is to understand the mechanisms that regulate the structure of blood vessels; a process we will term "vascular remodeling." Hypertension is a major risk factor for development of atherosclerosis (strong correlation between fatty streak formation and BP) and for clinical events (strong correlation between unstable angina, myocardial infarction, stroke and BP). Our major hypothesis is that hypertension is a major risk factor for atherosclerosis because the ability of the vessel to compensate for plaque burden (a process that requires outward vascular remodeling) is inhibited in hypertensive patients. We also suggest that impaired remodeling in hypertensives is due to 1) direct effects of elevated blood pressure, and 2) pressure-independent genes associated with essential hypertension that modulate the ability of the vessel to remodel. To gain insight into the mechanisms by which hypertension influences vascular remodeling we will selectively breed normotensive and hypertensive inbred rat strains that differ in their ability to remodel and perform a genetic analysis. Our preliminary data document significant differences in lumen diameter induced by blood flow among inbred rat strains. Our hypothesis is that among rats with genetic hypertension (e.g. SHR, SHR-SP, and Genetically Hypertensive rat of New Zealand (GH) there will be additional genetic determinants that modulate remodeling in response to physiologic stimuli such as flow. The use of genetic linkage analysis in the proposed project represents a novel approach to understanding the mechanisms that regulate vascular structure. Its advantage is that it is based on recombination probability, and requires no prior knowledge of the mechanisms to find the gene(s) that contribute to the process. We have developed and published a reproducible and quantitative model for flow-dependent vascular remodeling. Using this model to study inbred rat strains we have made the exciting preliminary observation that the remodeling abilities of Brown Norway (BN, high) and GH (low) strains differ by more than 2 standard deviations. Based on these data our major goal is to perform a BN x GH cross and total genomic scan to identify major genes that alter the ability of vessels to remodel in hypertension. Aim 1: Characterize the time course of flow- induced remodeling in the carotid arteries of Brown Norway rats (BN, high remodelers) and Genetically hypertensive rats (GH, low remodelers). Aim 2: Intercross GH and BN to obtain 200 F2 progeny that express a range of remodeling and blood pressure phenotypes. Aim 3: Genotype P0 and F2 rats and use interval mapping to determine the chromosomal location of the quantitative trait loci (QTL) that are responsible for flowinduced remodeling and blood pressure. Aim 4. Create a congenic strain of GH rats containing genes associated with high remodeling ability. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HEME-HEME OXYGENASE-CARBON MONOXIDE SYSTEM IN HYPERTENSION Principal Investigator & Institution: Johnson, Fruzsina K.; Tulane University of Louisiana New Orleans, LA 70118
34 Hypertension
Timing: Fiscal Year 2002; Project Start 20-SEP-2002; Project End 31-AUG-2007 Summary: Carbon monoxide (CO) can be endogenously formed during the enzymatic degradation of heme by heme oxygenase (HO). Although CO is generally regarded as a vasodilator, by its inhibitory effect on nitric oxide synthase it is also a vasoconstrictor. On high salt diet Dahl salt-sensitive rats (DS) develop hypertension that is accompanied by decreased NO formation. This project will investigate the role of the vascular hemeHOCO system in endothelial dysfunction during salt-induced hypertension in DS rats. The following specific aims will be addressed: Aim1: Characterize the temporal changes in various indeces of the HO system, arteriolar NO function, and cardiorenal pathologies in DS and salt-resistant (DR) rats on high and low salt diets. Aim2: Determine the effects of genetic predisposition for salt-sensitivity, high salt diet, and hypertension on various indeces of the HO system, arteriolar NO function, and cardiorenal pathologies in DS and DR rats. Aim3: Establish the effects of altered HO system function on artedolar NO function, and cardiorenal pathologies in DS and DR rats on high and low salt diets. Methods: Some animals will receive antinhypertensive treatment, others pressor treatment. Some groups will be treated with heme-L-lysinate, others with zinc protoporphyrin IX to increase or decrease endogenous CO formation, respectively. HbCO will be measured with a clinical grade analyzer (OSM3). Vascular HO-1 protein content will be studied by Western-blotting and immunohistochemistry (ABC method). NO function will be examined in isolated skeletal muscle arterioles by studying responses to a NO synthase inhibitor, an endothelium-dependent vasodilator, and a NO donor. Internal diameter of pressurized arterioles will be measured with a microscope and a video caliper. Objectives: These studies will provide information on temporal changes in HO function, cardiorenal pathologies and arteriolar NO function during salt-induced hypertension. Furthermore, they will evaluate the factors (genetic salt-sensitivity, high salt diet, and/or hypertension) contributing to HO-mediated NO dysfunction during salt-induced hypertension in DS rats. They will also examine the effects of altered endogenous CO formation on arteriolar NO function and cardiorenal injury in DS rats during salt-induced hypertension. Understanding the pathological basis of endothelial dysfunction may help to develop causetargeted therapy resulting in prolonged survival of hypertensive patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HEPARIN ON HYPOXIC PULMONARY HYPERTENSION AND REMODELING Principal Investigator & Institution: Hales, Charles A.; Professor of Medicine; Massachusetts General Hospital 55 Fruit St Boston, MA 02114 Timing: Fiscal Year 2001; Project Start 01-JUL-1987; Project End 31-MAY-2005 Summary: Thickening of the media with intrusion on the vascular lumen contributes substantially to the pulmonary hypertension seen in primary or secondary pulmonary hypertension. Heparin has been shown to be antiproliferative and antihypertrophic for systemic and pulmonary artery smooth muscle cells (PASMC) in vitro and has been variably effective at inhibiting in vivo remodeling in several systemic and pulmonary models. We have found that commercial heparin lots vary widely in their antiproliferative activity. However, an effective antiproliferative heparin in vitro for PASMC proliferation can prevent hypoxic pulmonary hypertension in mice, rats and guinea pigs and can reverse it in guinea pigs even in the presence of continued hypoxia. We have also shown that heparin's ability to inhibit PASMC proliferation and in vivo pulmonary hypertension correlates with its ability to prevent mitogen stimulation of the Na+/H+ antiporter. We have found that highly specific antagonists of the Na+/H+
Studies 35
antiporter such as dimethyl amiloride (DMA) can inhibit PASMC proliferation in response to growth factors in vitro and can substantially prevent hypoxic pulmonary hypertension and remodeling in rats. As we dissect the chemistry of antiproliferative heparins we have shown, among other things, that the protein core is unimportant and that 3-0-sulfate is not an important feature in full-length heparin. We have made new heparin derivatives by O-acetylating heparin with butanoyl and hexanoyl which are more potent antiproliferative agents on PASMC than native heparins and are nonanticoagulant. We have found that in PASMC heparin stimulates the production of the cell cyclin kinase inhibitors p21 and p27 which are inhibitors of cell proliferation in other cells. With this progress we hope to continue our pursuit of an effective treatment for pulmonary hypertension with the following specific aims: 1) Continue examining strongly versus weakly antiproliferative heparins in order to discover the reasons for the differences with a goal of amplifying the antiproliferative potency and perhaps divorcing it from the anticoagulative and osteopenic properties. 2) Determine in the pig, as a preclinical trial in a large mammal, if heparin or heparin fragments or the Na+/H+ inhibitor DMA are effective at preventing hypoxic pulmonary hypertension and 3) Determine if heparin's mechanism of action in preventing SMC proliferation is via stimulation of the cyclin kinase inhibitors p21 and p27. Thus, this proposal may lead to new therapeutic agents for humans with pulmonary hypertension and may elucidate a new understanding of how heparin prevents PASMC growth. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HYPERTENSION / ATHEROSCLEROSIS PARADIGMS Principal Investigator & Institution: Herrera, Victoria L.; Profesor of Medicine; Medicine; Boston University Medical Campus 715 Albany St, 560 Boston, MA 02118 Timing: Fiscal Year 2001; Project Start 15-AUG-1999; Project End 31-JUL-2003 Summary: Clinical and experimental data demonstrate unequivocally that hypertension accelerates atherosclerosis. This is an intriguing pathogenic phenomenon since the interaction is quite unambiguous for two complex diseases marked by clinical and genetic heterogeneity. Currently, the mechanisms underlying this interaction have not been elucidated. Strategic animal models are needed to mechanistically dissect pathogenesis. We have developed a transgenic hyperlipidemia- genetic hypertensive rat model by hepatic over-expression of human cholesteryl ester transfer protein (hCETP) in Dahl salt-sensitive (S) rats. Transgene high copy number in Tg[hCETP]53 Dahl S rats elicits aortic, coronary and intramyocardial atherosclerotic lesions and decreased life spans compared with no lesions in non-transgenic Dahl S controls and minor medial changes in Tg[hCETP]25 Dahl S rats with transgene moderate copy number. In this research proposal, we will investigate whether synergistic decrease of NO activity induced by both hypertension and atherosclerosis results in enhanced activated endothelial molecular and cellular changes which are then differentially amplified. as enhanced pro-inflammatory and pro-thrombotic changes leading to progressive vascular disease. The following specific aims will be studied: 1) Determined whether the endothelium of hypertensive, markedly hyperlipidemic Tg[hCETP]53 Dahl S rats exhibit exaggerated endothelial cell activation (marked by enhanced and/or sustained up- regulation of ICAM-1 and P-selectin gene expression and increased monocyte adhesion compared with control age-matched normotensive, markedly hyperlipidemic Tg[hCETP]53 Dahl salt-resistant (R) male rats, and control non-transgenic age-matched hypertensive, normolipidemic Dahl S rats. 2) Determine whether exaggerated activation results in amplified dysregulation through enhanced pro-inflammatory response (marked by increased TNF-alpha expression and increased NF-kappaB activation in
36 Hypertension
endothelial cells, macrophages) and/or pro-thrombotic response (marked by tissue factor TF expression in endothelial cells, macrophages, intimal smooth muscle cells)-distinct from corresponding arteries in control normotensive, markedly hyperlipidemic Tg[hCETP]53 Dahl R rats as well as in control hypertensive, normo-lipidemic Dahl S rats. 3) Define the hierarchical relationship of hypertension hyperlipidemia and decreased NO activity on the acceleration of atherosclerosis by determining which manipulation, high salt diet, Western Type Diet, or NO-inhibitor L-NA treatment will cause Tg[hCETP]25 Dahl S rats to exhibit similar atherosclerotic lesion phenotype similar to Tg[hCETP]53 Dahl S rats. 4) Define the mechanistic role of endothelial NO pathway in the interaction of hypertension and atherosclerosis; sufficient versus essential but not sufficient versus modifying but not essential by early, mid-point, and late-onset L-arginine treatment of Tg[hCETP]53 Dahl S rats and determine whether the acceleration of atherosclerosis by hypertension is differentially attenuated, if not significantly resolved. This research proposal will provide key information on mechanisms that underlie the acceleration of atherosclerosis by hypertension which will identify new strategies for intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INTEGRINS
HYPERTENSION
AND
ARTERIAL
INJURY--A
ROLE
FOR
Principal Investigator & Institution: Meininger, Gerald A.; Regents Professor and Associate Head; Medical Physiology; Texas A&M University Health Science Ctr College Station, TX 77843 Timing: Fiscal Year 2001; Project Start 15-AUG-1999; Project End 31-JUL-2003 Summary: The overall goal of this project is to test the prevailing hypothesis that hypertension and arteriosclerosis may be linked through a mechanism that involves oxidative stress. Our working hypothesis is that oxidative stress in hypertension and atherosclerosis acts to induce similar alterations in the expression of specific integrins and extracellular matrix (ECM) proteins that are responsible for changes in vasomotor function and vascular smooth muscle (VSM) phenotype. Our recent studies have established a novel link between VSM and endothelial integrins and the control of vascular tone. In addition, preliminary data indicates that oxidative stress can alter the expression of at least one of the VSM integrins linked to vasomotor activity and an ECM protein that is a ligand for this receptor. These altered integrin/matrix interactions may predispose the arterial wall to development of vascular pathology. This project incorporates a model of renal hypertension and atherogenesis that will be studied at various stages of disease development in large, intermediate and microvascular sized arterial vessels. Assessments will be made of the redox status, integrin and ECM profiles and vascular reactivity to soluble and insoluble integrin-binding ligands. These ligands will include synthetic Arginine-Glycine-Aspartic Acid (RGD) containing peptides and type I collagen and osteopontin, which are up-regulated following vascular injury. Our strategy is combining studies of intact vessels, cellular, biochemical and molecular approaches will provide a powerful approach for testing our hypothesis and systematically integrating our results, The specific aims are: Aim 1: Characterize the vasomotor response for large intermediate and small arterial vessels to known integrinbinding peptides, type I collagen and osteopontin at varius stages of development for a rat model of renal hypertension and/or imposed oxidative stress (allylamine treated). Vasoactivity will be correlated with measurements of redox status and integrin/ECM profiles. Aim 2: Characterize the vascular redox status and mechanisms leading to the development of oxidative stress in models of renal hypertension and atherogenesis and
Studies 37
evaluate the role of NFkappaB as a common signal transduction pathway. Aim 3. Characterize and evaluate changes in vascular ECM/integrin expression at the gene and protein levels that are associated with renal hypertension or oxidative stress and to define the influence of oxidative stress on extracellular matrix and integrin gene expression. These studies will provide new information that will advance our understanding vascular function in hypertension and atherosclerosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HYPERTENSION AND COLLAGEN: EFFECT OF AC-SDKP Principal Investigator & Institution: Rhaleb, Nour-Eddine; Internal Medicine; Case Western Reserve Univ-Henry Ford Hsc Research Administraion Cfp-046 Detroit, MI 48202 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2006 Summary: (provided by applicant): Hypertension causes left ventricular hypertrophy (LVH) and increased LV interstitial and perivascular collagen deposition. Increased cardiac collagen may alter function in hypertrophied hearts. Angiotensin converting enzyme inhibition(ACEi) has been shown to reverse LVH in hypertension. This effect has been attributed to blockade of angiotensin II (Ang II) formation and kinin degradation. We have shown that N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), another natural substrate for ACE, prevents LV monocyte/macrophage infiltration and fibrosis without altering blood pressure (BP) or LVH in hypertension. We believe this is the first demonstration that Ac-SDKP affects cardiac fibrosis; however, the mechanism(s) or receptor(s) by which Ac-SDKP affords cardioprotection are not known, nor whether Ac-SDKP contributes to the cardioprotective effects of ACEi. We hypothesize that (1) Ac-SDKP has an anti-inflammatory and antifibrotic effect on the heart in hypertension via specific receptor(s) linked to a cascade of signal transduction, including MAP kinase, protein kinase C (PKC), NF-kB and TGF-beta, and (2) the effect of ACEi on the heart is mediated in part by Ac-SDKP. In aim new analogues of AcSDKP and SDK fragments will be synthesized and tested to identify (1) an ACE-resistant analogue with an inhibitory effect similar to Ac-SDKP that can be radiolabeled and used to characterize Ac-SDKP receptor(s), and (2) an antagonist that specifically blocks the inhibitory effect of Ac-SDKP. In aim II we will determine whether (1) the effect of AcSDKP is linked to suppression of TGF-beta, CTGF and Smad expression, and (2) the effect of TGF-beta on collagen type I and/or III expression is affected by Ac-SDKP. We will also examine whether Ac-SDKP inhibits p38 and PKC activation in fibroblasts. In aim IV we will determine whether in vivo Ac-SDKP (1) inhibits inflammatory cell infiltration in the LV, p42/p44, p38 and/or PKC activity, NF-kB,TGF-beta, CTGF and Smads, (2) regresses cardiac fibroblast proliferation, collagen expression and synthesis, (3) increases matrix metalloproteinase activity, and (4) decreases cardiac expression of collagen I and III in rats with long-term hypertension. In aim IV we will examine whether the effect of ACE inhibitionon LV collagen deposition is mediated by Ac-SDKP. This project will provide important new information on the on the cardioprotective effect of ACEi in hypertension and the mechanism of action of Ac-SDKP. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HYPERTENSION IN AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE Principal Investigator & Institution: Schrier, Robert W.; Professor; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508
38 Hypertension
Timing: Fiscal Year 2001; Project Start 21-APR-2001; Project End 31-JUL-2001 Summary: Hypertension occurs commonly and early in the natural history of autosomal dominant polycystic kidney disease (ADPKD). Hypertension (HBP) has been shown to have an adverse effect on both patients and renal outcome in ADPKD. Moreover, left ventricular hypertrophy (LVH), a known risk factor for cardiovascular mortality and sudden death, occurs frequently in HBP ADPKD patients. At present it is not clear what is the optimal level of blood pressure reduction in HBP ADPKD patients to minimize loss of renal function or to reverse lVH. Given that hypertension is the most important treatable variable to affect renal and patients outcome in ADPKD, this project will determine in prospective longitudinal fashion the appropriate level of blood pressure control in HBP ADPKD patients. Secondly, since lVH also occurs in normotensive ADPKD patients, factors other than HBP or the ADPKD gene may play a role in the development of lVH in ADPKD patients. Given that activation of the renin-angiotensinaldosterone axis is important in ADPKD and that the deletion polymorphism of the angiotensin converting enzyme gene is associated with LVH, normotensive and HBP ADPKD patients with and without LVH will be studied with regard to the frequency of this genotype. As well, given that hypertension in the unaffected parent is associated with earlier and more frequent HBP in ADPKD patients, the frequency of the angiotensinogen gene variant M235T will also be studied with regard to onset of hypertension and frequency of preeclampsia in ADPKD patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HYPERTENSION, OXIDATIVE STRESS AND RACE Principal Investigator & Institution: Guo, Zhongmao; Meharry Medical College 1005-D B Todd Blvd Nashville, TN 37208 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-JUL-2006 Summary: Data from humans and animal models suggest that oxidative stress might play a part in the pathogenesis of hypertension. For example, patients and animals suffering from hypertension have been shown to increase reactive oxygen species (ROS) production and decrease antioxidant capacity. ROS, e.g., superoxide and hydrogen peroxide, have been shown to induce contraction and proliferation of vascular smooth muscle cells in vitro. The research described in this pilot project will examine the relationship between hypertension and oxidative stress in African-Americans. The goal of this study is to test the hypothesis that hypertension is associated with an increased oxidative stress, This project includes three specific aims: In specific aim 1, we will determine the relationship between hypertension and the concentration of plasma F2isoprostane (an in vivo oxidative stress marker) and the production of blood hydrogen peroxide and superoxide. In specific aim 2, we will determine the relationship between hypertension and the activities of major antioxidant enzymes, including superoxide dismutases, catalase and glutathione peroxidases, in blood. In specific aim 3, we will determine the relationship between hypertension and the activities of ROS-generating enzymes, including xanthine oxidase and NADH/NADPH oxidase, in blood, if the hypothesis described above is correct, hypertensive patients will show a higher level of F2-isoprostanes, a higher production of ROS, higher activities of ROS-generating enzymes and/or lower activities of antioxidant enzymes than normotensive subjects. In this pilot project, we will focus on African-Americans because hypertension is more prevalent in African-Americans than that in Caucasians. However, no unifying hypothesis as to the genetic mechanisms responsible for the excess prevalence of hypertension among African-Americans has emerged. If results from this pilot project show that hypertension is associated with an increased oxidative stress, we will
Studies 39
propose a study to compare the oxidative status of different populations, e.g., AfricanAmericans and Caucasians with or without hypertension, to test if the high prevalence of hypertension in African-Americans is associated with a high level of oxidative stress. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HYPOTHALAMIC ROLE IN HYPERTENSION Principal Investigator & Institution: Stern, Javier E.; Assistant Professor; Pharmacology and Toxicology; Wright State University Colonel Glenn Hwy Dayton, OH 45435 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 31-MAY-2006 Summary: (provided by applicant): This proposal focuses on the role of preautonomic neurons in the paraventncular nucleus (PVN) of the hypothalamus in the pathophysiology of hypertensive disorders. Hyperactivity of the sympathetic nervous system is commonly present in patients with essential hypertension, and the level of autonomic disbalance is a major determinant of patients' prognosis. By virtue of reciprocal connections with afferent visceroceptive and efferent motor autonomic centers, the PVN stands as a potential neural substrate underlying altered sympathetic drive in hypertension. Accumulating evidence implicates the PVN as an important component in the neuronal circuit involved in the pathophysiology of hypertension. In general, the cellular mechanisms involved in altered neuronal excitability during hypertension remain unknown. Since the PVN contains both preautonomic parasympathetic and sympathetic neurons, we propose to use it as a model to study altered cellular mechanisms contributing to unbalanced autonomic outflow, characteristic of hypertension. We hypothesize that the cellular properties of PVN preautonomic neurons innervating functionally different autonomic targets are differentially altered in hypertension, contributing to altered autonomic drive. Our preliminary data shows our ability to conduct experiments to test these hypotheses, and supports and altered function of these neurons in hypertension. Using a multifaceted approach combining in vitro electrophysiological recordings with immunohistochemical and in situ hybridization techniques we will answer the following questions: 1) What are the main intrinsic and extrinsic factors controlling neuronal excitability in PVN preautonomic neurons? 2) Are the cellular properties of PVN preautonomic neurons involved in the control of the parasympathetic and sympathetic autonomic function differentially affected during hypertension? 3) What are the cellular mechanisms underlying altered excitability during hypertension? Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: IDENTIFICATION HYPERTENSION
OF
GENES
INVOLVED
IN
HUMAN
Principal Investigator & Institution: Sheffield, Val C.; Professor; University of Iowa Iowa City, IA 52242 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-JAN-2006 Summary: The primary goal of this project is to identify genes and loci involved in hypertension and related phenotypes. Identification of genes involved in Mendelian disorders can rely heavily on genetic mapping and positional cloning strategies cloning strategies. However, identification of genes involved in complex inherited disorders (such as hypertension) by positional cloning alone is not likely to be highly successful. The multiple genes contributing to a complex phenotypes can allow genetic mapping, but prevent refinement of loci because recombinants cannot be unequivocally resolved from the influences of unlinked loci. Thus, identifications involved in complex
40 Hypertension
phenotypes requires the use of all available information and a combination of research approaches. Such information includes the temporal-spatial expression patterns of genes, studies of gene function, knowledge of sequence polymorphism of genes, data obtained from physiological studies in animal models, as well as positional information gained from genetic studies in humans and animal models. In this study, we will take a multifaceted approach to the identification of genes and loci potentially involved in hypertension and hypertension-related phenotypes. In specific aim 1, we will use expression data from rat models of hypertension and gene-expression profiles, along with human and rat positional data to identify high- probability candidate genes for human gene-expression profiles, along with human and rat positional data to identify high-probability candidate genes for human hypertension. Inj specific aim 2, the human orthologues of the high-probability candidate genes identified in specific aim I will be isolated and evaluated for allelic association with hypertension in human populations. In specific aim 3, we will verify and refine putative loci influencing body size phenotypes and blood pressure, and in aim 4, we will identify a gene causing a human Mendelian disorder influencing blood pressure. The study design is built upon our past successes and resource development. We will take full advantage of existing genomic resources, as well as resources that are rapidly becoming available including: the complete draft sequence of the human genome; the discovery efforts of our NIH-funded "Rat Gene Discovery and Mapping Program" at the University of Iowa; human/rat syntenic maps; extensive rat and human cDNA libraries enriched for full -length clones; microarray hybridization capabilities with a comprehensive set and human cDNA libraries enriched for full-length clones; microarray hybridization capabilities with a comprehensive set of rat ESTs; and efficient sequencing team; expertise in all facets of genotyping and genetic mapping; outstanding information management expertise; wellcharacterized rat hypertension models; and carefully-phenotyped human subjects. All of these resources will be used toward ensuring the successful completion of this project. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IMPROVING ADHERENCE TO BLOOD PRESSURE GUIDELINES Principal Investigator & Institution: Carter, Barry L.; Professor; Clinical and Administrative Pharmacy; University of Iowa Iowa City, IA 52242 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Blood pressure (BP) control in the U.S. is poor despite six sets of guidelines generated over the last 30 years. Poor adherence to guidelines may be due to inadequate systems to track and monitor patients and inadequate therapy adjustments by physicians. While various strategies exist to assist physicians with improving guideline adherence and achieving better BP control, a consistently effective approach to solving the problem has not been found. The longrange goal of the principal investigator is to develop and evaluate collaborative relationships between physicians and pharmacists that improve pharmaco-therapy. This will be a five-year, multi-center, study to evaluate the impact of physician/pharmacist collaborative teams on adherence to hypertension guidelines (JNC-VI) in six community-based family practice sites. There will be two study phases. Phase I comprises a needs assessment to identify barriers to guideline adherence and design intervention implementation refinement strategies. Phase II will be a prospective, randomized trial to assess the impact of physician/pharmacist collaborative teams on hypertension guideline adherence and BP control. The specific aims of Phase I are to: 1) identify the scope and nature of physician and patient variables that may contribute to
Studies 41
poor guideline adherence and 2) to refine the intervention implementation strategy and design tools for assessing guideline adherence and barriers to adherence. The specific aims of Phase II are: 1) to determine if there is a change in guideline adherence and knowledge of hypertension when physicians are involved in physician/pharmacist teams and 2) to determine if physician/pharmacist teams can achieve better BP control compared to usual care. We expect that the improvement in guideline adherence and reduction in BP with this intervention will significantly impact patients with hypertension. Because there are more than 37 million Americans with uncontrolled hypertension, this model has to potential to become an important strategy to help achieve the BP goals for Healthy People 2010. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IMPROVING HYPERTENSION
THE
TREATMENT
AND
CONTROL
OF
Principal Investigator & Institution: Margolis, Karen L.; Minneapolis Medical Research Fdn, Inc. 600 Hfa Bldg Minneapolis, MN 55404 Timing: Fiscal Year 2001; Project Start 01-JUN-1999; Project End 31-MAY-2004 Summary: Candidate: Karen Margolis, M.D., M.P.H., is a member of the Berman Center for Outcomes and Clinical Research at the Minneapolis Medical Research Foundation, and staff physician at Hennepin County Medical Center, a teaching hospital affiliated with the University of Minnesota. Dr. Margolis is interested in finding interventions which bring patients, physicians and the system of care together to implement effective medical care, specifically in the area of cardiovascular disease prevention. Career Objectives. Dr. Margolis' immediate career objectives include: (1) advanced course work in epidemiology, biostatistics, health services research, study design and analysis; (2) work with the Berman Center multi-center clinical trials and prospective studies; (3) work with mentor to develop and evaluate research direction, skills and experience; (4) obtain funding for and implement pilot and full-scale studies of randomized trial of physician incentives for improving the control of hypertension in a managed care organization; and (5) develop other related research projects. Dr. Margolis' long-term career objectives include attaining independence as an investigator in the field of patient-oriented cardiovascular disease prevention research and incorporating the theme of physician and patient adoption of effective interventions in a system of care for the prevention of cardiovascular disease morbidity and mortality. Research Plan. During the five year period of the award, Dr. Margolis plans to undertake at least one major clinical trial preceded by a pilot study for that trial. The clinical trial and pilot study are entitled "Program for Improving the Treatment and Control of Hypertension (PITCH)" and will involve testing the hypothesis that clinics in a managed care organization receiving funding to design their own program for improving the control of hypertension will have a higher percentage of hypertensives with controlled blood pressure compared to both clinics given similar funding for financial incentives (provided directly to physicians based on performance) and control clinics given no financial incentives. Dr. Margolis also has planned several other related projects which include: (1) study of patient attitudes towards physician financial incentives and satisfaction with care in PITCH; (2) study of impact of physician financial incentives in PITCH on medical care other than hypertension; and (3) the role of patient health state preferences in acceptance of hypertension treatment and control of hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
42 Hypertension
•
Project Title: INDUCED HYPERTENSION FOR ACUTE ISCHEMIC STROKE Principal Investigator & Institution: Wityk, Robert J.; Neurology and Neurosurgery; Johns Hopkins University 3400 N Charles St Baltimore, MD 21218 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAR-2005 Summary: (provided by the applicant): Thrombolysis using intravenous tissue Plasminogen Activator (rtPA) is the only proven therapy for Acute Ischemic Stroke, but it is only appropriate for some patients. The long-term goal of this proposal is to investigate the use of induced Hypertension as an alternative means of Cerebral Reperfusion. The rationale assumes the presence of an Ischemic Penumbra, a region of hypoperfused brain that is still viable and able to be rescued. Until recently, delineation of the Ischemic Penumbra in clinical practice has been impractical. Diffusion-Weighted MRI (DWI) allows early detection of Ischemic injury and Perfusion-Weighted MRI (PWI) shows areas of relative Cerebral Hypoperfusion. The DWI/PWI mismatch (in patients with PWI > DWI) can be functionally defined as the Ischemic Penumbra. Pharmacological elevation of blood pressure may increase cerebral blood flow to this region, and allow recovery of function. Before a double-blind, placebo-controlled clinical trial can be undertaken; several scientific issues need to be addressed. We propose a pilot clinical trial using DWI/PWI to investigate the physiology of induced Hypertension, and also study whether MRI can be used as a means of selecting patients likely to respond to treatment, as improved selection will allow more efficient trials later. Patients presenting within 12 hours of onset of stroke will be treated with a protocol of intravenous phenylephrine to increase mean arterial pressure to a maximum of 30% over baseline. Patients will have DWI/PWI studies performed before and during induced Hypertension, as well as 1-month follow-up. Serial neurological assessments (including the NIH stroke scale) will be performed by an investigator blinded to the imaging studies. The specific aims of this proposal are to: 1) determine the proportion of patients who have clinical improvement or serious adverse events related to induced Hypertension; 2) determine if the presence of DWI/PWI mismatch identifies patients likely to respond to induced Hypertension. We hypothesize that patients with mismatch are more likely to respond than are patients with other MRI patterns; and 3) correlate changes in neurological deficit with changes in MRI during induced Hypertension. An association of improved function, with reduction in the volume of mismatch, will support the proposed physiology. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: INOS GENE TRANSFECTION IN PULMONARY HYPERTENSION Principal Investigator & Institution: Chicoine, Louis G.; Pediatrics; University of New Mexico Albuquerque Controller's Office Albuquerque, NM 87131 Timing: Fiscal Year 2001; Project Start 01-APR-1999; Project End 31-MAR-2004 Summary: Pulmonary hypertension (PH) is a significant cause of morbidity and mortality affecting a broad range of patients. Neonatal pulmonary hypertension is the second leading cause for admission to neonatal intensive care units for respiratory support. In adults, PH causes significant morbidity and mortality in patients with chronic obstructive pulmonary disease. In all patients, PH is characterized by cellular proliferation and altered vasoreactivity in the pulmonary vascular bed. The objectives of this proposal are to evaluate the vasodilator efficacy and toxicity of NO produced by virally mediated inducible nitric oxide synthase (iNOS) gene transfection in the lung and to determine the effect of virally transfected iNOS on the pathogenesis of PH. The general hypothesis is that virally transfected iNOS will result in sufficient NO formation
Studies 43
to modulate pulmonary vasoconstriction and attenuate pulmonary vascular changes associated with pulmonary hypertension, but insufficient NO formation to result in toxicity. Utilizing human iNOS gene and, as a control, the E. coli lac Z reporter gene coding for beta-galactosidase (beta-gal) adenovirus constructs our goals set forth in this proposal are: 1) to optimize iNOS gene delivery and expression in the rat lung, 2) to determine the role of transfected iNOS on the development of pulmonary hypertension, and 3) to compare intravascular and intratracheal delivery of the iNOS gene in terms of gene expression, vascular reactivity and toxicity. These goals are addressed in the following specific aims: Specific Aim number 1: Assess the effectiveness of adenovirusmediated iNOS gene transfection in attenuating acute pulmonary vasoconstrictor responses. Specific Aim number 2: Assess iNOS gene transfection-mediated effects on the development of chronic hypoxia-induced pulmonary hypertension. Specific Aim number 3: Assess the efficacy and toxicity of intravascularly and intratracheally administered adenoviral iNOS constructs. The methods will involve using adenovirus constructs containing the gene for iNOS or beta-gal that will be administered intravascularly; the lungs will then be studied to determine vascular reactivity, NO production, and localization of transfected iNOS. Some rats will be transfected and exposed to chronic hypoxia. Finally, intravascular and intratracheal delivery will be compared in terms of gene localization and toxicity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISMS FOR CARDIOVASCULAR CONTROL EARLY IN DIABETES Principal Investigator & Institution: Brands, Michael W.; Associate Professor; Medical College of Georgia 1120 15Th St Augusta, GA 30912 Timing: Fiscal Year 2003; Project Start 01-JAN-1997; Project End 31-MAR-2007 Summary: (provided by applicant): We have shown that hyperglycemia at the onset of Type I diabetes causes significant hypertension if it is induced in rats with chronic blockade of nitric oxide synthesis. The hypertension is prevented by blocking angiotensin II, or the sympathetic nervous system; but our data suggest the two systems are linked in this response and may involve superoxide and thromboxane. Blood pressure and nitric oxide also track closely with GFR. The studies in this proposal will test the central hypothesis that nitric oxide protects against hypertension at the onset of diabetes by counteracting pressor actions of the sympathetic and renin-angiotensin systems. The Specific Aims are: 1) to test the hypothesis that nitric oxide protects against AngII-induced hypertension at the onset of diabetes by: a) chronically clamping (fixing) renin-angiotensin system activity at normal levels;b) blocking AngII action in rats with chronic intravenous and intrarenal i) ramipril and ii) iosartan; c) blocking AngII action in mice with ACE gene knockout; d) determining if gradual onset of diabetes causes the same renin secretion and blood pressure responses; e) determining whether low sodium intake increases the dependence of blood pressure on nitric oxide. 2) to test the hypothesis that the SNS contributes to the hypertensive response primarily through renal mechanisms. We will: a) determine the roles of a versus b receptors in mediating the renal, renin, and blood pressure responses:b) remove the renal nerves to test the role of the kidney in mediating the sympathetic pressor effect; c) determine if a decrease in ANG II is required for adrenergic blockade to prevent the hypertension; d) determine if the SNS effect is due to increases in SNS activity, or whether it plays a permissive role, 3) to test the hypothesis that nitric oxide counteracts AngII-dependent superoxide and thromboxane production to control blood pressure at the onset of diabetes. We will determine this by: a) "blocking" superoxide with a superoxide dismutase mimetic in rats
44 Hypertension
and gene overexpression in mice; b) quantifying the degree to which AngII determines whether superoxide significantly affects blood pressure: c) determining if thromboxane receptor blockade will decrease blood pressure if superoxide is not increased: d) determining whether knockout of superoxide dismutase 1 exacerbates the hypertensive response. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MENTORED DEVELOPMENT AW
PATIENT-ORIENTED
RESEARCH
CAREER
Principal Investigator & Institution: Gurubhagavatula, Indira Md; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, PA 19104 Timing: Fiscal Year 2001; Project Start 01-AUG-2000; Project End 31-JUL-2005 Summary: PROPOSAL (Adapted from the applicant's abstract): Characterized by intermittent airway closure during sleep, OSA is extremely prevalent, afflicting 2-4% of Americans. If left untreated, a large body of evidence convincingly shows that OSA can lead to daytime hypertension. In fact, 20-30% of patients with OSA will have hypertension, and 40% of patients with hypertension have occult OSA. The question then is how to identify patients who have OSA from among this high-risk population of individuals with hypertension. Polysomnography (PSG), the current diagnostic gold standard, is expensive and inconvenient. Several simple techniques to screen for OSA are available: questionnaires, craniofacial measurements, nocturnal oximetry and airflow monitoring devices. However, no one has compared their relative efficacies or costs in one unified population. The investigator proposes to compare these screening tools against full PSG's in a cohort of patients at high risk for OSA, i.e., outpatients with hypertension. Among the cases of OSA subsequently identified, the applicant next proposes to evaluate outcomes of treatment of OSA with continuous positive airway pressure (CPAP) in a randomized, placebo- controlled trial. The specific aims, therefore, are: 1) to compare the accuracy of several screening strategies for OSA in outpatients with hypertension; 2) to determine their relative economic costs; and 3) to determine the effect of CPAP therapy on blood pressure (BP) and sympathetic activity during sleep and awake states in OSA patients with hypertension. These projects are extraordinarily important. They have the potential to lead to dramatic changes in the approach to management of the patient with hypertension. Along with a complementary program of didactic training, they will constitute a strong foundation of experience for the applicant in her goal of becoming an independent clinical investigator. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MICROVESSEL HYPERTENSION
O2
RESPONSES
IN
SALT-SENSITIVE
Principal Investigator & Institution: Lombard, Julian H.; Professor; Physiology; Medical College of Wisconsin Po Box26509 Milwaukee, WI 532264801 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): Alterations in local blood flow control mechanisms may play a major role in the transition from an elevated cardiac output to a maintained elevation in vascular resistance in volume-expanded forms of hypertension. An enhanced constriction of arterioles, in response to increased O2, availability has been demonstrated in many forms of hypertension, but little is known regarding the mechanisms that mediate O2-induced constriction of microvessels. Cytochrome P450 (CYP450) 4A omega-hydroxylase, which catalyzes the formation of 20-HETE (a
Studies 45
vasoconstrictor metabolite of arachidonic acid), may act as an 02 sensor in the microcirculation. This study investigates the role of CYP450 4A omega-hydroxylase and 20-HETE in mediating O2-induced constriction of arterioles in the microcirculation of the Dahl S rat, a genetic model of salt sensitive hypertension, and in SS.BN13 consomic rats, in which chromosome 13 of the normotensive Brown Norway rat is substituted into the Dahl S genetic background. The SS.BN13 consomic rats are 98% identical to the Dahl S rat genetically, but do not exhibit elevated blood pressure in response to high salt diet. The overall hypothesis to be tested is that the enhanced response of arterioles to elevated PO2 in Dahl S hypertensive rats is due to one or a combination of 3 factors: increased 20-HETE production, increased sensitivity of arterioles to the vasoconstrictor effects of 20-HETE, and/or altered expression of CYP450 4A omega-hydroxylase. The effect of 20-HETE inhibition, on arteriolar responses to elevated PO2 will be determined in the in situ cremaster muscle of Dahl S and SS.BN13 rats on high salt (HS) and low salt (LS) diets. Cytochrome P450-4A omega-hydroxylase isoforms in arterioles and parenchymal cells of Dahl S rats and SS.BN13 rats on high and low salt diets will be assessed by RT-PCR and Western blotting, and changes in 20-HETE production in response to elevated PO2 will be measured in arterioles and parenchymal cells. Arteriolar constriction in response to exogenous 20-HETE will also be compared in the in situ microcirculation of Dahl S rats and SS.BN13 rats on high salt and low salt diets for various periods of time. These studies should provide an increased understanding of how the mechanisms that regulate vascular tone during changes in 02 availability, are altered during hypertension and during increases in dietary salt intake Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MORPHOLOGY AND FUNCTION OF BRAIN VESSELS Principal Investigator & Institution: Baumbach, Gary L.; Professor; Pathology; University of Iowa Iowa City, IA 52242 Timing: Fiscal Year 2003; Project Start 01-APR-1978; Project End 31-MAR-2007 Summary: (provided by applicant): Two provocative concepts have recently emerged in relation to mechanisms that contribute to altered cerebral vascular structure during chronic hypertension. First, superoxide, and its regulation by superoxide dismutase(s) (SOD), may play a critical role in regulating vascular structure by interacting with nitric oxide and by participating in cellular signaling and gene regulation. Second, the reninangiotensin system may play an important role in regulating vascular structure both by generating superoxide and by directly activating specific receptors. The overall objective of this proposal is to utilize novel molecular approaches to examine the roles of superoxide and the renin-angiotensin system in altered cerebral vascular structure in chronic hypertension. The proposed studies address two specific aims. The first aim is to clarify the influence of superoxide and SOD on cerebral vascular hypertrophy in chronic hypertension. To test the hypothesis that oxidative stress during chronic hypertension may contribute to cerebral vascular hypertrophy, effects of pressureoverload (induced by transverse aortic banding) will be examined using in vivo methods to assess vascular mechanics, histological methods to define hypertrophy, and biochemical methods to quantitate superoxide levels in carotid arteries and cerebral arterioles of genetically-altered mice that are deficient in the NADPH oxidase subunit, gp91phox, and that overexpress CuZn-SOD. Cerebral vessels also will be examined in these genetically- altered mice with arteriovenous fistulae to test the hypothesis that oxidative stress may contribute to cerebral vascular hypertrophy during increases in arterial pulse pressure, independently of increases in mean pressure. These studies will be among the first to use in vivo approaches to explore the influence of superoxide on
46 Hypertension
vascular structure. The second aim is to examine the role of angiotensin II in cerebral vascular remodeling during chronic hypertension. Vascular remodeling (defined as reduction in external diameter) plays an important role in hemodynamic alterations associated with essential hypertension in humans. Genetically altered mice that overexpress human renin (R+) and human angiotensinogen (A+) will be used to test the hypothesis that angiotensin II contributes to remodeling of cerebral arterioles independently of increases in arterial pressure. In addition, R+/A+ mice that are deficient in gp91phox will be generated to test the hypothesis that remodeling of cerebral arterioles in response to overproduction of angiotensin II may depend, at least partly, on the generation of superoxide. Finally, R+/A+ mice will be treated with blockers of angiotensin II type 1 and type 2 receptors to examine the hypothesis that remodeling of cerebral arterioles may be mediated by activation of one or both of these receptor types. These studies should provide important new insight into the mechanisms of vascular remodeling. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NEDD4-DEPENDENT REGULATION OF ENAC IN HYPERTENSION Principal Investigator & Institution: Snyder, Peter M.; Associate Professor of Medicine; University of Iowa Iowa City, IA 52242 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-JAN-2006 Summary: The epithelial Na+ channel (ENaC) is a distal target of the renin- angiotensinaldosterone pathway, where it is critically positioned to play an important role in blood pressure control. Gain-of-function mutations in ENaC cause Liddle's syndrome, an inherited form of hypertension. Conversely, loss-of-function mutations cause a genetic disorder of salt wasting and hypotension (pseudohypoaldosteronism type 1). Thus, an understanding of the function and regulation of this channel will provide important insights into human blood pressure variations and the pathogenesis of hypertension. In this project, we are responsive to Goal 2 of the RFA; "mechanistic studies on the consequence of genetic variation." In preliminary studies, we found that the interaction of ENaC with Nedd4, a ubiquitin protein-ligase, plays an important role in controlling Na+ absorption. Several findings suggest that a ubiquitin protein-ligase plays an important role in controlling Na+ absorption Several findings suggest that Nedd4 might play a critical role in the control of blood pressure. First, in preliminary studies we found that Nedd4 decreases ENaC Na+ current by targeting the channel for degradation. First, in preliminary studies we found that Nedd4 decreases ENaC Na+ current by targeting the channel for degradation. Second, the sequences in ENaC that bind to Ndd4 (PY motifs) are deleted or mutated in Liddle's syndromes. Third, we found that Liddle's syndrome mutations in the betaENaC subunit prevention Nedd4 from inhibiting the channel. Thus, the overall goal of this proposal is to understand the molecular mechanisms by which Nedd4 from inhibiting the channel. Thus, the overall goal of this proposal is to understand the molecular mechanisms by which Nedd4 inhibits ENaC, and to begin to define the role of this pathway in Liddle's syndrome and more common forms of hypertension. Thus, the overall goal of this proposal is to understand the molecular mechanisms by which Nedd4 inhibits ENaC, and to begin to define the role of this pathway in Liddle's syndrome and more common forms of hypertension. In the first two specific aims, we will investigate the molecular determinants for the inhibition of ENaC by Nedd4. Specific Aim 1 will focus on the role of a C2 domain in Nedd4 in the Ca2+- dependent inhibition of ENaC, and on the physical interaction between WW domains in Nedd4 and the PY motifs of ENaC. Specific Aim 2 will complement Aim 1, determining the sequences in ENaC that are
Studies 47
involved in the interaction and inhibition by Nedd4. Specifically, we will examine the role of the PY motifs that are targeted in Liddle's syndrome, and test the hypothesis that ubiquitination of ENaC is required for Nedd4- mediated inhibition. In Specific Aim 3, we will examine the functional consequences of natural genetic variation in ENaC found in hypertensive populations. This may provide important new insight into the role of ENaC and Nedd4 in human blood pressure variation and the pathogenesis of hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NEURAL MECHANISMS OF LONG-TERM CARDIOVASCULAR CONTROL Principal Investigator & Institution: Osborn, John W.; Professor; Animal Science; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, MN 554552070 Timing: Fiscal Year 2001; Project Start 15-SEP-2000; Project End 31-JUL-2004 Summary: (Verbatim from Applicant's Abstract): Many forms of hypertension are exacerbated by increased dietary salt (salt-dependent hypertension) but the mechanisms are unknown. The overall objective of this proposal is to investigate the autonomic and hemodynamic mechanisms of salt-dependent hypertension. In preliminary experiments the applicants continuously monitored mean arterial pressure (MAP), heart rate (HR) and cardiac output (CO) in intact (SHAM) and sinoaortic denervated (SAD) rats consuming normal and high salt diets. Increasing dietary salt for two weeks resulted in an immediate and sustained increase in total peripheral resistance (TPR) in SHAM rats, but not hypertension since both HR and CO were decreased. In SAD rats, an equivalent salt-induced increase in TPR was observed, but CO and HR did not fall and saltdependent hypertension resulted. These results led to the following hypotheses and specific aims. Experiments in Specific Aim 1 will test the hypothesis that increased dietary salt stimulates release of neuropeptide-Y (NPY) from sympathetic vasomotor neurons to cause vasoconstriction in normotensive rats. In protocol 1, the response of hemodynamics (MAP, CO, HR and TPR) and plasma NPY to increased dietary salt in normal rats and rats chronically treated with the NPY Yl receptor antagonist BIPP 3266 will be measured. The effect of BIPP 3266 on the hemodynamic responses to salt will also be studied in rats chronically treated with alpha and beta-adrenergic antagonists, which have been shown to modulate the vasoconstrictor activity of NPY. In protocol 2, the effect of renal and splanchnic denervation on NPY mediated renal and mesenteric vasomotor responses to increased dietary salt respectively will be determined. In these same animals, the applicants will examine vascular Yl receptor MRNA expression using RT-PCR and correlate these findings with vascular sensitivity to NPY. Experiments in Specific Aim 2 will test the hypothesis that chronic salt induced decreases in cardiac output are mediated by baroreflex control of cardiac sympathetic and vagal tone. To test this hypothesis cardiac output, heart rate and arterial pressure will be monitored 24 hours/day in intact and baroreceptor denervated rats consuming normal and high salt diets. Power spectral analysis of heart rate will be preformed to assess the effect of increased salt on cardiac vagal and sympathetic activity throughout the experiment. In these same rats, the effect of long-term pharmacological blockade of M2 muscarinic receptors and beta l adrenergic receptors on cardiac vagal and sympathetic tone respectively (heart rate power spectra), cardiac output and arterial pressure will be examined before and during dietary salt loading. The applicants predict that impaired autonomic control of the heart will result in salt-dependent hypertension due to failure to buffer salt-induced vasoconstriction by a decrease in cardiac output. These experiments will provide important novel information on the role of the autonomic
48 Hypertension
nervous system in the long-term control of hemodynamics under conditions of increased dietary salt. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NEW EXPERIMENTAL MODELS OF HYPERTENSION Principal Investigator & Institution: Kurtz, Theodore W.; Professor; Laboratory Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, CA 94122 Timing: Fiscal Year 2002; Project Start 01-JAN-1997; Project End 31-DEC-2006 Summary: (provided by the applicant): The spontaneously hypertensive rat (SHR) is the most widely studied animal model of essential hypertension and has been a valuable tool for studying the pharmacology and physiology of blood pressure control. However, despite 30 years of research with this model, the primary mechanisms responsible for hypertension in the SHR remain undefined. Recently, we have succeeded in trapping a quantitative trait locus (QTL) for hypertension within a narrow segment of chromosome 8 in a unique congenic strain of SHR. In the current studies, we will exploit this congenic strain together with proven strategies of genome wide expression analysis and meiotic mapping to identify the molecular lesion(s) responsible for the effect of this region of chromosome 8 on blood pressure. We will pursue two alternative hypotheses using complementary strategies as follows: Hypothesis 1. A hypertension gene exists within the target segment of chromosome 8 that is differentially expressed between the SHR and the SHR congenic strain in one of the major organs suspected to be involved in the primary pathogenesis of spontaneous hypertension (brain, adrenal gland, or kidney). Accordingly, we will search for candidates for hypertension within the target chromosome segment by screening for genes that are differentially expressed between these organs of the SHR and the SHR congenic strain and that map back within the congenic segment of chromosome 8. Hypothesis 2. A hypertension gene exists within the target segment of chromosome 8 that is not differentially expressed between the SHR and the SHR congenic strain. To cover for this alternative possibility, we will also narrow the location of the hypertension gene by meiotic mapping analysis of a segregating F2 population derived from the SHR progenitor strain and the SHR congenic strain that carries the target region of chromosome 8 from the BN strain. Hypertension candidate genes will then be isolated using cDNA screening techniques to identify genes expressed in the brain, adrenal gland, or kidney that map within this chromosome region. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NMR STUDIES OF CYTOSOLIC METAL IONS AND OXIDATIVE STRESS Principal Investigator & Institution: Gupta, Raj K.; Professor; Physiology and Biophysics; Yeshiva University 500 W 185Th St New York, NY 10033 Timing: Fiscal Year 2003; Project Start 01-MAY-1982; Project End 31-AUG-2007 Summary: (provided by applicant): Our long-range goal is to elucidate the role of intracellular mineral ions (Na+, K+, free Mg2+ & free Ca2+) and oxidative stress in the pathophysiology of essential hypertension and type 2 diabetes. We seek to understand how the regulation of intracellular concentrations of essential metal ions and membrane lipids goes astray in health disorders, especially hypertension and diabetes. Our main research tool is NMR spectroscopy. Our laboratory played a key role in the development of NMR methods for measuring various intracellular cations and we also have
Studies 49
considerable expertise in the use of 1H NMR for analyzing membrane phospholipid composition and the degree of membrane fatty acid unsaturation (double bonds) and average chain length. Oxidative stress, which may play a contributory role in the pathogenesis of diabetes as well as hypertension, causes peroxidative degradation of membrane lipids resulting in a loss of fatty acid double bonds that can be quantitated by 1H NMR. The following specific aims will be pursued: (1) To investigate the mechanism of altered renal sodium homeostasis in salt-sensitive hypertension; (2) To demonstrate that oxidative stress, which results in overproduction of reactive oxygen species (ROS), can cause loss of unsaturation in fatty acyl chains of membrane phospholipids as measured by 'H NMR, and to test the hypothesis that peroxidative degradation of lipids as measured by loss of membrane fatty acid unsaturation during oxidative stress results in intracellular ionic changes similar to those seen in essential hypertension; (3) To investigate a possible protective role of magnesium against oxidative stress and whether there is a decrease in antioxidant capacity, as measured by glutathione (GSH) levels, in tissues exposed to low Mg environment; (4) To test the hypothesis that a deficit in membrane fatty acid unsaturation is associated with human essential hypertension and to investigate if there is an alteration in sphingomyelin-ceramide pathway in hypertension; (5) To find out if impairment of nitric oxide synthesis by inhibition of nitric oxide synthase, which causes hypertension in a normal rat, produces membrane lipid changes similar to those seen in essential hypertension; (6) To test the hypothesis that hyperglycemia causes peroxidative degradation,of membrane lipids as measured by 1H NMR, especially in vascular tissue, and, if so, whether hyperglycemia associated loss of fatty acid unsaturation and intracellular ionic alterations can be reversed by dietary antioxidants such as vitamin C and E; (7) To investigate increased vulnerability of hypertensive as well as hyperglycemic kidney and myocardium to ischemic damage and its relationship to increased perexidative degradation of membrane lipids; and (8) To design, develop and test a method for non-invasive measurement of "intracellular sodium using triple-quantum filtered (TQ)23 Na NMR. The proposed NMR investigations of intracellular ions and oxidative stress in hypertension and hyperglycemia condition may eventually lead to better strategies for the management of these health disorders. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NONINVASIVE ASSESSMENT OF PRIMARY PULMONARY HYPERTENSION Principal Investigator & Institution: Shandas, Robin; Professor; Pediatrics; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 31-MAY-2005 Summary: (Applicant's Abstract): This proposal addresses the problem of evaluating the efficacy of newly developed agents for the treatment of primary pulmonary hypertension. The use of catheter techniques to measure pulmonary vascular resistance severely limits routine evaluation of such treatments. We propose to develop, refine and test a non-invasive ultrasound based means of accurately evaluating pulmonary vascular resistance in children with primary pulmonary hypertension. The hypothesis for this project is based on the relationship between changes in downstream impedance within a fluid system and the characteristics of the pressure pulse propagation wave that develops within the arterial walls. We propose to show that downstream impedance affects the pulse propagation wave traveling within the main pulmonary artery and that changes in downstream impedance, as would occur with treatments such as inhaled nitric oxide or infused prostaclyin, can be followed by measuring pulse
50 Hypertension
propagation characteristics. Furthermore, we propose that the pressure pulse propagation in the main PA affects local velocities, and that such changes in local velocities can be quantified as a velocity propagation using non-invasive ultrasound color M-mode imaging. This should significantly aid in evaluating new treatments for primary pulmonary hypertension and thereby expand treatment options and improve quality of life for patients. The aims of this project, therefore, are: 1. Demonstrate analytically that a fundamentally rooted mathematical and physical foundation exists for using velocity data to extract pressure pulse propagation characteristics for pediatric primary pulmonary hypertension. 2. Develop and test a method for using color Mmode velocity data to predict downstream impedance using highly reproducible in vitro models. 3. Determine clinical utility of the color M-mode approach using existing clinical protocols studying the efficacy of nitric oxide and/or 100 percent 02 treatment in the catheterization laboratory to reduce pulmonary vascular resistance in children with primary pulmonary hypertension. 4. Determine whether color M-mode measured velocity propagation (Vel-prop) predicts pulmonary vascular resistance in the clinical situation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: OXIDATIVE STRESS AND GENETICS OF PREHYPERTENSION Principal Investigator & Institution: Nesbitt, Shawna D.; Internal Medicine; University of Texas Sw Med Ctr/Dallas Dallas, TX 753909105 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2005 Summary: (provided by applicant): High normal blood pressure in increasingly recognized as an important cardiovascular risk factor in part due to the likelihood of progression to hypertension. However, there is considerable heterogeneity in the risk of hypertension; some individuals progress while others maintain or regress. Thus, clinicians are unable to identify those at highest risk. Further, the effect of treatment of high normal blood pressure (BP) on the progression to hypertension is unknown. Consequently, my colleagues and I designed the Trial of Preventing Hypertension (TROPHY) as a prospective randomized placebo controlled trial of short-term monotherapy with the angiotensin receptor blocker (ARB) candesartan cilexitil in 809 subjects with high normal BP. Trophy provides a unique opportunity to study the mechanisms of the progression to hypertension. Emerging basic research emphasizes the role of superoxide (.O2-) as a major mechanism by which chronic exposure to low concentrations of angiotensin II (All) includes progressive hypertension. Via interaction with All receptors in the vessel wall, All activates NAD(P)H oxidases producing .O2and other reactive oxygen species that a) quench nitric oxide (NO), leading to NO deficient hypertension and b) stimulate signaling of vascular smooth muscle cell growth. TROPHY provides a new opportunity to translate this basic research from animal models to the clinical setting. Major Mechanistic Hypothesis: All receptor mediated generation of .O2- both quenches NO and stimulates vascular hypertrophy, and thereby constitutes the major mechanism of progression to hypertension from high normal BP. Specific Aims: Utilizing the TROPHY trial of 800 subjects on placebo or short-term ARB treatment we will: 1) in the placebo group, determine if individuals with high normal BP and high oxidative stress levels (F2 isoprostanes and glutathione ratio) are at high risk for progression to hypertension; 2) in the ARB group, determine if short-term treatment lowers oxidative stress levels compared to placebo and if the level of oxidative stress predicts failure to progress to hypertension; and 3) determine genetic sequence variants in the All, oxidative stress, and NO pathways associated with progression to hypertension or failure to progress to hypertension.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: OXIDATIVE STRESS AND SYMPATHETIC NERVE ACTIVITY Principal Investigator & Institution: Campese, Vito M.; Medicine; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, CA 90033 Timing: Fiscal Year 2003; Project Start 24-JAN-2003; Project End 31-DEC-2006 Summary: (provided by applicant): Hypertension is a common manifestation of renal disease and greatly contributes to its progression as well as to cardiovascular morbidity. Clearly, hypertension is an important etiology in the pathogenesis of renal failure. In the United States, hypertension is the primary cause of end-stage renal disease in approximately 29 percent of dialysis patients. In conjunction with other diseases such as diabetes and chronic glomerulonephritides, hypertension, when uncontrolled, hastens the progression of renal disease. Cardiovascular disease is the leading cause of death in patients receiving maintenance hemodialysis and hypertension is considered the most important factor responsible for cardiovascular events in these patients. Adequate BP control may reduce the progression of renal disease and cardiovascular morbidity in these patients, but often this is difficult to achieve with currently available drugs. The old paradigm is that hypertension in renal disease is the result of activation of the reninangiotensin system and/or volume expansion. Our studies strongly support the notion that a renal injury may result in activation of renal afferent pathways that integrate with the central nervous system, and lead to stimulation of efferent SNS activity and hypertension. Locally produced angiotensin II in the brain in response to these afferent stimuli seems to be responsible for SNS activation through inhibition of nitric oxide. Our hypothesis is that angiotensin-II activation of ROS may reduce NO availability in key brain region and result in increased SNS activity in a model of neurogenic hypertension caused by renal injury developed in our laboratory. To test this hypothesis we will pursue 3 specific Aims: 1. Test the hypothesis that locally produced Ang II mediates the activation of central SNS activity caused by phenol-renal injury. To this end, we will measure Ang II concentration in the dialysate collected from the PH using the microdialysis technique, and the expression of renin mRNA in the posterior hypothalamus. 2. Test the hypothesis that radical oxygen species (ROS) activated by Angiotensin II down-regulate nitric oxide production in the brain resulting in increased SNS activity. To this end, we will measure the concentration of reactive oxygen species (ROS) in the hypothalamus or rats with the phenol-renal injury or rats infused with Ang II in the lateral ventricle. In addition, we will evaluate the effects of anti-oxidants, or scavengers of ROS, and Ang II AT1 receptor antagonists on BP, sympathetic activation and ROS concentrations in the hypothalamic region. 3. Test the hypothesis that increased ROS production may result in NO inhibition and SNS activation in other forms of experimental hypertension, such as the DOCA-sait model, and the renovascular hypertension model. If our hypothesis were to be correct, administration of inhibitors of the renin-angiotensin system particularly if combined with antioxidants should result in better control of BP in these models. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: P450 EICOSANOIDS AND RENAL FUNCTION IN HYPERTENSION Principal Investigator & Institution: Roman, Richard J.; Professor; Physiology; Medical College of Wisconsin Po Box26509 Milwaukee, WI 532264801 Timing: Fiscal Year 2001; Project Start 01-JUL-1986; Project End 31-MAR-2005
52 Hypertension
Summary: (Adapted from the Investigator's Abstract): Recent studies have indicated that cytochrome P450 (CYP) metabolites of arachidonic acid (AA), in particular 20HETE, play a central role in the regulation of renal tubular and vascular function and the long-term control of arterial pressure. During the last funding period, this investigator identified a gene of the cytochrome P4504A family that is differentially expressed in the kidney of Dahl S and Lewis rats and that cosegregates with the development of hypertension in an F2 cross of Dahl S and Lewis rats. To further explore the role of this system in the control of renal function, they have developed (in collaboration with Dr. J. Rapp) congenic strains of rats in which overlapping segments of chromosome 5 of the Lewis rat, that include or exclude the P4504A region, have been introgressed into the Dahl S genetic background by greater than 8 generation of selective back-cross breedings. They now propose to determine whether the P4504A genes play a causal role on altering renal function and/or the development of hypertension and glomerulosclerosis in Dahl S rats by: 1) comparing blood pressure, renal function and the expression of P4504A enzymes in congenic strains of rats in which the P4504A alleles of normotensive Lewis rats have been introgressed into the Dahl S genetic background; 2) determining whether selective intrarenal blockade of the formation of 20-HETE can "rescue" the hypertensive and renal phenotypes in P4504A congenic Dahl S rats; 3) cloning and sequencing the 5'-flanking regions of the P4504A2 and 4A3 genes to determine whether there are sequence variants that can explain the differences in the expression of these genes in the outer medullas of the kidneys of Dahl S and Lewis rats. These studies will provide important new information regarding the role of P450 metabolites of AA in the regulation of renal function and will determine whether this pathway plays a primary or secondary role in the development of hypertension and/or glomerular disease in Dahl S rats. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HYPERTENSION
PHARMACOGENETIC
THERAPY
OF
PULMONARY
Principal Investigator & Institution: Li, Song; Pharmacology; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, PA 15260 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2007 Summary: (provided by applicant): Pulmonary hypertension is a significant clinical entity severely affecting the longevity and quality of life for patients with either primary or secondary' forms of this disorder. Regardless of its underlying cause, pulmonary hypertension remains intractable to traditional pharmacotherapy. Recent basic genetic and preclinical pharmacological] studies suggest that newly developed agents modifying endothelin activity may have a potential role in pulmonary hypertension. Nonetheless, it is highly likely that general principles of pharmacology predictive of issues of non-specificity and adverse effects as well as target alterations leading to tachyphylaxis and desensitization will ultimately limit the use of new generation endothelin modifiers. In the current proposal, we suggest that advances in non-viral based genetic therapy may provide novel alternatives to traditional pharmacotherapy. In particular, delivery of antisense Oligodeoxynucleotides (ODN) to endothelin-1 lET-l) by immunoliposome can be used to down regulate pulmonary' endothelial ET-1 biosynthesis and similar application with RNA/DNA chimeric oligonucleotide may more permanently silence such expression. Accordingly, specific aims of this comprehensive proposal are: Aim 1: To develop an oligonucleotide-based approach to achieve efficient down-regulation of ET-1 in endothelial cells. ODN scanning arrays and ET-1 ELISA will be employed to identity - antisense ODNs that are highly efficient in
Studies 53
inhibiting the ET-1 expression in mouse lung endothelial cells. In addition, RNA/DNA chimeric oligonucleotides will be investigated as an approach to achieve a long-term silencing of ET-1 in pulmonary endothelium. Aim 2: To develop novel delivery, systems to achieve efficient delivery of oligonucleotide to pulmonary endothelium with reduced toxicity. Aim 3: To investigate the biological effect of tissue-specific down-regulation of ET-1 in normal mice and in mice with PHT. The current proposal will lead to a better understanding of the roles of ET-1 in mouse hypoxia-induced pulmonary hypertension and provide experimental and preclinical support for rational pharmacogenetic approach to pulmonary hypertensive disorders. Down regulation of ET-1 biosynthesis by pulmonary endothelium by immunoliposome-mediated delivery of ODN may by itself, or in combination with" direct pulmonary vasorelaxants (e.g. nitric oxide and oxygen), provide an approach to prevent the progressive pathological aspects of PHT and ameliorate return towards more normal pulmonary vascular structure and function. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PILOT--DEPRESSION HYPERTENSIVES
&
TREATMENT
ADHERENCE
IN
Principal Investigator & Institution: Rojas, Mary; Mount Sinai School of Medicine of Nyu of New York University New York, NY 10029 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: Hypertension is a prevalent disorder. Treatment for hypertension usually requires a patient to take daily medications, reduce sodium intake and lose weight, adhere to routine follow-up visits, and undergo routine monitoring tests. Adherence to such regimens requires a great degree of patient motivation and perseverance, convictions that often require strong feelings of self-efficacy. Hypertensive patients who are also depressed may be less likely to summon the necessary self-discipline to follow such a complex health routine. Depression is also a prevalent disorder; approximately 9.5% of U.S. adults ages >=18 suffer from a depressive disorder in any given year. The relatively high prevalence of these 2 conditions suggest that it is likely that both hypertension and depression will occur concomitantly. Current research is lacking on the extent to which depression complicates hypertension and adherence to antihypertensive treatment regimens. Specific Aims: 1) To describe the prevalence of depression among controlled and uncontrolled hypertensive minority patients; 2) To describe the prevalence of treatment adherence among depressed and nondepressed hypertensive patients; 3) To explore associations between depression, treatment adherence, and blood pressure control; 4) To assess the feasibility of recruiting minority hypertensive patients to undergo screening for depression. We will take advantage of an ongoing AHRQ-EXCEED-funded randomized trial among minority patients with uncontrolled hypertension and utilize the recruitment procedures and tools to identify minority patients with diagnosed and treated hypertension. We will assess patients for depression, anti-hypertensive treatment adherence and perceived self-efficacy. We will survey 30 controlled and 30 uncontrolled hypertensive minority patients recruited from the waiting rooms of clinics in East and Central Harlem. This pilot study is an exploration of the relationship of depression, attitudes toward treatment of depression, hypertension treatment adherence, self-efficacy and blood pressure control. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
54 Hypertension
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Project Title: PILOT--DOPAMINE RECEPTOR ASSOCIATED PROTEINS AND HYPERTENSION Principal Investigator & Institution: Jones, John E.; University of Virginia Charlottesville Box 400195 Charlottesville, VA 22904 Timing: Fiscal Year 2002; Project Start 01-SEP-1997; Project End 31-AUG-2007 Summary: Genetic hypertension may be the result of abnormalities in the renal dopaminergic system. The renal autocrine/paracrine natriuretic function of dopamine, via the D1-like receptors (D1 and D5), is impaired in the spontaneously hypertensive rat. The impairment is not the result of a decrease in renal dopamine production nor is it due to abnormalities in the G proteins or effector proteins. We propose that the impairment resides within one or more intermediate components. Genetic changes occurring within the genes that encode D1-like receptor interacting proteins may lead to disruption of D1-like receptor mediated signal transduction and, in turn, result in increased risk for the development of hypertension. Specific aim 1 will identify and characterize the proteins that interact with the D1-like receptors in the kidney. We will employ the yeast two- hybrid system to identify genes encoding proteins that interact with the D1-like receptors. The D1 and D5 dopamine receptors will be divided into structural domains consisting of the amino terminal, carboxy terminal, extracellular and intracellular loops and each of the seven transmembrane segments. These domains will be used as molecular probes to detect interactions occurring with proteins expressed from a human kidney cDNA library. Protein-protein interactions will be verified using laser confocal microscopy and fluorescence resonance energy transfer techniques. Specific aim 2 will test the hypothesis that there are differences in the sequences of the D1-like receptor interacting proteins between normotensive and hypertensive individuals and that it is these differences that lead to hypertension. Genetic variants, especially those occurring within regions identified in specific aim 1 as potential sites of interaction with the D1-like receptor proteins or those that map to regions of the human genome associated with hypertension risk, will be studied further. We will screen for polymorphisms in genomic DNAs derived from control and hypertensive individuals representing several different ethnic groups including Asians, Africans, American Caucasians, and Italian Caucasians. Finally, specific aim 3 will determine if there are differences in the expression of D1-like receptor interacting proteins in young and adult kidney during maturation. A greater understanding of the proteins and protein networks associated with the regulation of the D1-like dopamine receptors will likely lead to greater insight into the roles these receptors play in the maintenance of blood pressure. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PILOT--THE BETA 2 ADRENERGIC RECEPTOR AND GENETIC HYPERTENSION Principal Investigator & Institution: Xu, Jing; University of Virginia Charlottesville Box 400195 Charlottesville, VA 22904 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2007 Summary: Abnormalities of beta2-adrenergic receptor (beta2-AR) function have been found in human essential hypertension and animal models of genetic hypertension. Mice with disrupted beta2- AR genes and their regulators are in loci associated with hypertension and genetic variations of beta2-AR are associated with hypertension. Beta2-ARs increase cAMP production, Na+/K+ATPase activity, and sodium transport; a decrease in these actions can cause the increased vascular reactivity in hypertension,
Studies 55
However, a decrease in beta2-AR function in renal tubules should lead to sodium loss, which potentially could lead to a decrease in blood pressure, offsetting the effect on vascular reactivity. The overall hypothesis is that in the kidney beta2-AR single nucleotide polymorphisms (SNPs) do not lead to sodium loss because sodium/hydrogen exchanger (NHE)-3 activity is increased in the kidney. We hypothesize that renal NHE3 activity is increased in subjects with beta2-AR SNPs because of an increased binding affinity of variant beta2-ARs to the NHE regulatory factor (NHERF). This leads to a decrease in NHERF available to inhibit NHE3 activity. Specific aim 1 will determine whether the interaction between beta2-AR in a heterologous expression system. We will determine whether genetically hypertensive rats have beta2-ARs SNPs. Even if there are no beta2-AR SNPs in genetically hypertensive rats, the reported increase in beta2-ARs in the kidney in genetically hypertensive rats may still result in increased binding of NHERF with the same consequences as variant beta2-ARs. Therefore, we will also quantify beta2-ARs, NHERF, and NHE3 protein in renal tubules and determine whether the binding of beta2-ARs to NHERF is increased in genetically hypertensive rats. Preliminary data indicate that the activity of a G protein-coupled receptor kinase, GRK6, is increased in renal proximal tubule cells of spontaneously hypertensive rats (SHR) compared with their normotensive controls, Wistar-Kyoto (WKY) rats. Because GRK6 can phosphorylate both beta2-AR and NHERF, specific aim 2 will determine if GRK6 activity in renal proximal tubules is, indeed, increased in SHR. We will also determine if the phosphorylation of beta2-ARs and NHERF is increased in SHR and whether such an increase is caused by increased GRK6 activity. Finally, the mechanism of the increased GRK6 activity in SHRs will be determined. These studies should allow us to determine the role of aberrant beta2-AR regulation of NHERF in genetic hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PRENATAL AND PERINATAL PROGRAMMING OF ADULT HYPERTENSION Principal Investigator & Institution: Vehaskari, Vesa M.; Director; Pediatrics; Louisiana State Univ Hsc New Orleans New Orleans, LA 70112 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 31-MAY-2006 Summary: (provided by applicant): Low birth weight is a risk factor for the development of human essential hypertension. The goal of the project is to define the mechanisms by which prenatal and perinatal factors program later hypertension. An experimental rat model of adult hypertension associated with low birth weight has been validated by preliminary experiments and will be used for all studies. The hypothesis is that pre- and perinatal hormonal imprinting irreversibly alters the sodium handling characteristic of the maturing kidney, resulting in sodium retention, expansion of extracellular volume (ECV), and hypertension. The studies will focus on the renal reninangiotensin system (RAS) and the cortical collecting duct (CCD) which are critical regulators of sodium balance. The following potential mechanisms will be investigated: ECV will be measured to test the hypothesis that it is expanded during the development of hypertension. Persisting upregulation of intrarenal RAS and failure to regress normally after birth would lead to sodium retention. This will be examined by determining the intrarenal expression of the RAS components at different time points before and after the development of hypertension by molecular biology methods; renal and systemic angiotensin I and angiotensin II contents will also be measured. CCD sodium transport is hypothesized to be upregulated due to prenatal imprinting of the angiotensin II type 1 receptor, the 11-beta-hydroxysteroid dehydrogenase enzyme,
56 Hypertension
and/or the mineralocorticoid receptor in this nephron segment. Isolated CCDs will be used to study the sodium transport rate and the expression of the specific genes and proteins involved in the Na transport pathway. To assess the contribution of reduced Na filtration to the development of hypertension, total nephron number as well as whole kidney and single nephron filtration rate will be measured; also, the total nephron number will be manipulated using prenatal retinoic acid treatment. Based on preliminary experiments, the hypothesis that the development of prenatally programmed hypertension can be modified or prevented during a postnatal window will be tested. The effect of short-term postnatal dietary and phamacological manipulations on the long-term blood pressure profile will be investigated. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PROSTACYCLIN SYNTHASE AND PROSTACYCLIN RECEPTOR IN PH Principal Investigator & Institution: Geraci, Mark W.; Director, Gene Array Facility; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2001; Project Start 17-SEP-2001; Project End 31-JUL-2006 Summary: (provided by applicant) Severe pulmonary hypertension, including primary pulmonary hypertension (PPH), is an important clinical problem with few clinical treatment options. The chronic, intravenous infusion of prostacyclin (PGI2) has been established as the treatment of choice for patients with PPH. It is now clear that longterm benefits occur which obviate the need for transplant in many cases. The physiological effects of prostacyclin on platelet behavior, vascular tone control, and cell proliferation are well established; however, we do not know whether prostacyclin effects the vascular remodeling in chronic pulmonary hypertension. Our overall hypothesis is that prostacyclin, through membrane-receptor dependent and independent mechanisms, is an important modulator of pulmonary vascular remodeling. We have demonstrated loss of the prostacyclin receptor (PGIR) protein in the smooth muscle cells of precapillary resistance arteries in patients with PPH. We postulate that impairment of the prostacyclin signal transduction contributes to pulmonary vascular remodeling. We have generated transgenic animals with selective pulmonary prostacyclin synthase (PGIS) overexpression. These animals are protected from the development of hypoxic pulmonary hypertension, and show no acute vasoconstriction or chronic vascular remodeling. In contrast, PGIR knockout (KO) mice, in response to hypoxia, develop rapid pulmonary hypertension accompanied by vascular remodeling. Microarray analysis of the lungs from the transgenic animals demonstrates a change in the global pattern of gene expression, which may be responsible for the "protected" phenotype, including changes in PPARs and COX-2. Our underlying concept is that PGI2 exhibits both membrane-receptor mediated and nuclear-receptor-mediated actions. These alternative mechanisms could include direct effects on gene expression, signaling pathways not yet recognized, or changes in the level of other eicosanoids. Our goal is to examine, using both animal models and cell systems, the effects of PGIS and PGIR on vascular smooth muscle cell (VSMO) growth and differentiation. In Specific Aim 1, we will determine whether pulmonary vascular tone and remodeling are mediated through the PGI2 receptor using bitransgenic mice with PGIS overexpression, but lacking PGIR. Specific Aim 2 is designed to define the effect of PGIS and PGIR on the growth and remodeling of vascular smooth muscle cells. The results of this work are designed to elucidate new potential therapeutic targets for
Studies 57
treating pulmonary hypertension, and broaden our understanding of vascular pathology in general. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PULMONARY HYPERTENSION FOLLOWING INTERMITTENT HYPOXIA Principal Investigator & Institution: Fagan, Karen A.; Medicine; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2007 Summary: (provided by applicant): Pulmonary hypertension (PHTN) is common in diseases characterized by chronic hypoxia (CH) (i.e. COPD, IPF) and occurs in 15-40% of patients with sleep apnea. Intermittent hypoxia (IH) mimicking the hypoxiareoxygenation cycles of sleep apnea causes systemic hypertension and altered regulation of systemic vascular tone. However, the effect of intermittent hypoxia on the pulmonary circulation is unknown. Recently, patients with sleep apnea-induced PHTN were found to have exaggerated hypoxic pulmonary vasoconstriction. Unlike in chronic hypoxia, hypoxia in sleep apnea is not continuous, thus the mechanisms causing sleep apnea-induced PHTN are likely different from chronic hypoxia-induced PHTN. We therefore hypothesize that intermittent hypoxia leads to pulmonary hypertension by differential expression of genes important in regulating pulmonary vascular tone. Specifically, we hypothesize that oxidant stress in IH increases NOS and decreases SOD leading to PHTN through increased formation of peroxynitrite thus decreasing NO available for cellular effects such as attenuating vasoconstriction and mediating vasodilation. We further hypothesize that IH activates redox sensitive transcription factors leading to differential lung gone expression compared to CH. We will present data showing IH-induced PHTN in both rats and mice. We also will present data showing differential expression of NOS (nitric oxide synthase) and SOD (superoxide dismutase) in the lung following IH compared to CH, which may contribute to IHinduced PHTN through increased oxidant stress and decreased NO activity. This proposal will address the questions: 1) does repetitive hypoxia-reoxygenation causes pulmonary hypertension, 2) that despite increased NOS, NO appears to be insufficient to prevent IH-induced PHTN, 3) decreased SOD may contribute to IH-induced PHTN by increasing oxidant stress and formation of peroxynitrite, and 4) does IH leads to differential gene expression through activation of specific signaling pathways compared to CH. We will correlate physiologic measures of PHTN and pulmonary vascular tone with expression and activity of NOS and SOD, measurements of oxidant stress and NO, and activation of specific signaling pathways leading to altered gone expression in IH. This proposal, for the first time, will identify the consequences of IH in the pulmonary circulation. Understanding mechanisms contributing to the development of PHTN in IH may lead improved cardiovascular morbidity and mortality in this common disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PULMONARY HYPERTENSION IN SCD Principal Investigator & Institution: Johnson, Cage S.; Professor of Medicine; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, CA 90033 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 31-MAR-2008 Summary: Chronic lung disease and pulmonary hypertension are complications of the sickle diseases that are increasingly recognized and are associated with considerable morbidity and mortality. Standard therapy with oxygen and a hypertransfusion
58 Hypertension
regimen have not demonstrated efficacy in prolonging survival in such patients, indicating a need for new approaches to management. Both hydroxyurea and L-arginine have the potential for increasing endogenous production of NO within the pulmonary vasculature and may have beneficial effects on oxygenation and pulmonary vascular resistance in patients with chronic lung disease and pulmonary hypertension. In addition, hydroxyurea improves red blood cell hemorheological properties and microvascular blood flow and thus combined therapy may impact smooth muscle hyperplasia in damaged pulmonary microvasculature. We hypothesize that beneficial clinical responses may accrue to patients with sickle chronic lung disease and pulmonary hypertension as a result of increases in NO generated by oral administration of hydroxyurea and/or L-arginine. We further hypothesize that these beneficial effects are consequent to modulation of vasoactive peptides (ET-1) and adhesion molecules (ICAM-I, V-CAM-I). The proposed research project is a phase II, randomized clinical trial designed to determine the effect of the NO donor L-arginine and hydroxyurea, either singly or in combination, on the biologic and clinical features of sickle cell disease patients with chronic lung disease and pulmonary hypertension. We further propose to characterize the effects of this treatment strategy on a broad range of RBC and hemorheologic properties in SCD,and to determine its efficacy in ameliorating chronic lung disease and pulmonary hypertension in these patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION ON SODIUM PUMPS IN THE KIDNEY Principal Investigator & Institution: Mcdonough, Alicia A.; Professor; Physiology and Biophysics; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, CA 90033 Timing: Fiscal Year 2001; Project Start 01-JUL-1984; Project End 31-JUL-2002 Summary: (Adapted from the applicant's abstract) - Previous results from the principle investigator's laboratory and other have shown that a rapid increase in mean arterial blood pressure inhibits salt and fluid reabsorption in the renal proximal tubule. The resulting increase in volume flow to the thick ascending limp of the loop of Henle provokes an increased sodium reabsorption and Na, k-ATPase activity to limit the increase in volume flow to the distal tubule and increase in Na-K-2Cl co- transporter. A defect in the proximal tubular or thick ascending limb of the loop of Henle (TALH) responses could be responsible for the reduced pressure natriuresis that is that is the hallmark of hypertension. The overall goal of the research is to test the hypothesis that the "downstream shift" of sodium reabsorption from proximal tubule (PT) to the TALH during acute hypertension is due to inhibition of PT sodium transporters, specifically NHE-3 and Na, K-ATPase), and that similar changes are evident in chronic genetic hypertension. There are three specific aims. Specific Aim 1 aims to determine the cellular mechanisms responsible for the decrease in proximal tubular sodium transport during acute hypertension. The principal investigator will investigate the mechanism of sodium pump inhibition and whether or not apical sodium transporters are themselves inhibited or move to sub-apical endosomal compartments. Specific Aim 2 is to determine the cellular mechanisms responsible for the increase in TALH sodium transport during acute hypertension Four questions will be addressed, namely, what is the mechanisms for sodium pump activation; is NHE-3 and/or NKCC2 activated or moved to the apical membrane; does a change in volume flow without hypertension activate sodium pump activity; and is cytochrome P450 arachidonic acid metabolism required for the response? Specific Aim 3 is to test the hypothesis that the cellular mechanisms responsible for the downstream shift in sodium reabsorption during acute
Studies 59
hypertension are evident in genetic models of hypertension. For these studies, the principal investigator will use spontaneously hypertensive rats known to have defective proximal tubular sodium transport regulation, and Milan hypertensive rats known to have elevated thick ascending limp Na, K- ATPase. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RENAL DOPAMINE-1 RECEPTOR DEFECT IN HYPERTENSION Principal Investigator & Institution: Jose, Pedro A.; Professor of Pediatrics; Pediatrics; Georgetown University Washington, DC 20057 Timing: Fiscal Year 2001; Project Start 25-JUL-1991; Project End 31-MAR-2005 Summary: (Verbatim from the application): There are abnormalities in dopamine (DA) production and receptor function in genetic hypertension: some DA receptor genes and their regulators are in loci linked to hypertension. Data generated during the previous funding period show that in mice disruption of the D dopamine receptor. one of the two D1 -like receptors, produces hypertension via a multireceptor cascade. The absence of the D5 receptor increases hypothalamic oxytocin (OT) secretion, sensitizes central V1 vasopressm receptors. activates central non-NMDA receptors and stimulates the sympathetic nervous system. D5 receptor disruption also leads to the generation of reactive oxygen species (ROS) that participate in the increase in BP. Renal tubular effects of D1 -like agonists are also impaired in D5 receptor mutant mice. Abnormalities in the D5 receptor may have functional significance in human essential hypertension because certain single nucleotide polymorphisms (SNPs) of the D5 receptor do not generate cAMP. SNPs of G protein-coupled receptor kinase 4y (GRK4y) and protein phosphatase 2A regulatory subunit, B56a, acting on the D1 receptor in the renal proximal tubule and medullary thick ascending limb cause a subset of genetic hypertension. Thus, D1 and D5 receptor dysfunction produces hypertension by renal and non-renal mechanisms. The overall objective of this proposal is to determine the mechanisms by which dysfunction of the D5 receptor increases system blood pressure. There are 4 specific aims: the first 2 deal with D5 receptor interactions with other G protein-coupled receptors while the last 2 deal with D5 receptor regulation of ROS production. Specific aim 1 will test the hypothesis that disruption of both D1 and D5 receptors results in a greater impairment in the ability to excrete a sodium load and greater increase in BP than disruption of either DA receptor alone, Specific aim 2 will determine the precise roles of oxytocin and V1 receptors in generating the hypertension in the D5 knockout mice. Specific aim 3 will determine the role of ROS in the pathogenesis of hypertension in D5 receptor mutant mice. The induction of heme oxvgenase- I (HO- 1) normalized BP in D5 receptor mutant mice. We will test the hypothesis that hypertension in D5 receptor mutant mice is caused, in part, by increased generation of ROS because of the mutant D5 receptor. per Se. and/or activation of OT/V1 receptors. Specific aim 4 will test the hypothesis that desensitized D5 and D1 receptors and certain D5 receptor SNPs couple to Ga13 instead of Gsa resulting in increased generation of ROS and renal Sodium transport. These studies should shed light into the relative contributions of a genetic D5 receptor abnormality and other G protein-coupled receptors (OT and V1) in the pathogenesis of genetic hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RENAL HYPERTENSION
HUMORAL
FACTORS
IN
RENAL
FUNCTION
&
Principal Investigator & Institution: Romero, Juan C.; Professor/Physiology & Biophysics; Mayo Clinic Rochester 200 1St St Sw Rochester, MN 55905
60 Hypertension
Timing: Fiscal Year 2001; Project Start 01-JUN-1979; Project End 31-JUL-2004 Summary: (Adapted from the Investigator's Abstract): The goal is to investigate the mechanisms by which the renin-angiotensin system (RAS) causes changes in intrarenal perfusion and tubular filtration-reabsorption dynamics. Renal artery stenosis in swine is predicted to stimulate angiotensin II (Ang II) production that stimulates superoxide isoprostane and endothelin (ET) production. Regional production of these vasoconstrictor agents will cause cortical ischemia with relative preservation of medullary perfusion. Electron beam computerized tomography (EBCT), a non-invasive x-ray, 3-dimentional tomographer (Imatron c-150) with high temporal resolution, has been developed recently and will be used to define changes in intrarenal blood flow and tubular flow patterns. A computerized analysis of vascular casts of microfil will help localize changes in the microcirculation. Aim # 1 examines changes in intrarenal hemodynamics and relate them with components of the RAS / oxidative stress cascade and ET in the stenotic and contralateral kidneys of pigs with 2-kidney-1-clip Goldblatt hypertension. Aim # 2 determines if reestablishing blood flow to the stenotic kidney normalizes renal blood flow and its intrarenal distribution in both the stenotic and control kidneys. Unclipping is expected to rapidly normalize arterial pressure is related to changes in the RAS and pressure natriuresis. Aim # 3 assesses intrarenal hemodynamics and status of the RAS/oxidative stress cascades in humans with focal unilateral renovascular stenosis. The human results are compared with measures in the swine model of 2-kidney-1 kidney clip hypertension.Aim # 4 examines swine with 2 kidney and 1 kidney clip hypertension with interventions to dissect causal relations between the RAS and / or oxidative stress and intrarenal flows. Aim # 5 is to characterize hypertension in swine produced by low dose Ang II infusion and the roles of oxidative stress and ET in the pathogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RISK OF HEART DISEASE/CANCER IN AFRICAN AMERICANS Principal Investigator & Institution: Robinson, Elwood L.; Professor; North Carolina Central University 160 Alexander-Dunn Bidg. Durham, NC 27707 Timing: Fiscal Year 2002; Project Start 01-JUN-1977; Project End 31-DEC-2005 Summary: The long-term goal of this study is to provide both cross-sectional and longitudinal data on psychosocial, behavioral and psychophysiological risk factors for cardiovascular disease and cancer in alumni of North Carolina Central (NCCU) in Durham, NC. This study represents one of the first examinations of the relationship between SES, age and gender and health risk factors in college-educated African Americans, and how these risk factors and their association may change over time. The primary purpose of this initial study is to conduct a telephone survey of 3,000 male and female NCCU alumni from three cohorts to examine social, behavioral, and psychological processes that mediate the well- known association between SES and hypertension. This study will also explore the association of age, gender and psychosocial factors with cardiovascular reactivity in a smaller subsample of 300 alumni. Finally, this study will investigate the association of SES, age and gender with cancer (in older persons), and with cancer-related risk factors and health behaviors. The following specific hypotheses will be tested: 1. Lower SES will be associated with a higher prevalence of hypertension and cancer (in older persons), and more hypertension and cancer risk factors. Lower SES will also be relate to fewer behaviors associated with cancer prevention and detection. 2. There will be age differences in the influence of SES on hypertension prevalence, and on hypertension and cancer risk factors, such that the SES effect will be stronger in the middle-aged than in elderly
Studies 61
respondents. 3. Psychological, behavioral and psychophysiological factors will mediate or moderate the association between SES and hypertension and cancer in adult blacks. These factors include social support, religious participation, residential environment, health care utilization, smoking physical activity, alcohol intake, dietary patterns, John Henryism, perceived stress/racism, optimism, depression, cancer knowledge/attitudes, screens behaviors and anger. Thus, we hope to show that the association of SES and hypertension and cancer can be partially explained by these variables. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RODENT MODEL OF SEVERE PULMONARY HYPERTENSION Principal Investigator & Institution: Tuder, Rubin M.; Associate Professor; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2001; Project Start 17-SEP-2001; Project End 31-JUL-2006 Summary: (provided by applicant): This project replaces the R01 grant: "VEGF protects against pulmonary vascular remodeling". Endothelial cell (EC) dysfunction plays an important role in the development of severe pulmonary hypertension (SPH). We have proposed that one of the most characteristic cellular features of SPH is the finding of EC clusters (tumorlets) in medium-size pulmonary arteries. Since these proliferated ECs express markers of angiogenesis, we have postulated that this EC growth occurs due to disordered angiogenesis. The VEGF receptor 2 (VEGFR-2) regulates several fundamental properties of ECs that impact on EC survival and nitric oxide and prostacyclin. We hypothesize that VEGF has a central role in the maintenance of the pulmonary endothelium. In this revised proposal, we seek to demonstrate that the blockade of the VEGFR-2 in combination with chronic hypoxia or monocrotaline causes severe pulmonary hypertension. We postulate that the combination of VEGFR-2 blockade and chronic hypoxia promotes death of normal pulmonary ECs and the selection of an abnormal, apoptosis-resistant, proliferating EC. Our experimental approach is based on in vivo studies with mice and rats with hypoxia- and monocrotaline-induced pulmonary hypertension (PH), ex vivo, in isolated perfused rat lungs, and, in vitro, using endothelial and lung smooth muscle cell cultures. Specifically, we propose to answer whether: 1. VEGF receptor blockade with SU5416 or ZK202650 in rats exposed to normoxia, or chronic hypoxia, or monocrotaline causes severe pulmonary hypertension associated with EC proliferation; and 2. The combination of VEGF receptor 2 blockade and chronic hypoxia leads to EC injury and EC death prior to the development of EC proliferation and SPH. Since we have successfully completed many of the originally planned experiments, we now propose experiments to confirm the specificity of our findings with SU5416 with a second, chemically unrelated VEGF receptor blocker, ZK202650, and we further probe the impact of abnormal VEGF/VEGF receptor signaling in the development of pulmonary hypertension in the transgenic mice expressing only the 188 amino-acid form of VEGF(VEGF188/188 mice) (Aim 1). In addition, we develop a novel approach to test whether apoptosis of normal lung ECs induces an apoptosis-resistant EC and SPH (Aim 2). This rodent model shares several of the key cellular and molecular features with human SPH. This proposal will allow us to better understand the natural history of human SPH associated with EC proliferation (secondary PH, project I and how alterations in pulmonary EC function affect pulmonary vascular tone and VSMC growth and hypertrophy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
62 Hypertension
•
Project Title: ROLE HYPERTENSION
OF
NA+
TRANSPORTER
GENES
IN
ESSENTIAL
Principal Investigator & Institution: Ruiz-Opazo, Nelson; Asociate Professor; Medicine; Boston University Medical Campus 715 Albany St, 560 Boston, MA 02118 Timing: Fiscal Year 2002; Project Start 15-JAN-1998; Project End 31-MAR-2006 Summary: (provided by applicant): Although there has been significant progress in the investigation of the genetic basis of hypertension, much work remains to be done against the cumulative backdrop of persistent clinical mandates. In essence, essential hypertension remains a highly prevalent disease and remains a major risk factor for the top causes of mortality in the USA: coronary artery disease, heart failure, arrhythmias. stroke and renal disease. It has become clear that (1) gene interaction must be factored into the genetic analysis of complex genetic diseases, (e.g., essential hypertension); and that (2) gene interaction analysis in well-controlled animal model experiments coupled to prioritized subsequent testing in genetically isolated human populations provides a robust experimental strategy. These realizations along with insights, observations, as well as experimental approach validation obtained in the previous research proposal, provide us with the clinical and scientific mandates to investigate the following hypothesis: The unidirectional gene interaction of a1 Na,K-ATPase (a1NK) and Na,K,2C1-cotransporter (NKC) genes increasing susceptibility to hypertension identified in Dahl S rats by an intercross linkage analysis reflects an in vivo molecular interdependence of these transporters and as such it should be amenable to in vivo testing via strategic transgenic experiments. Accordingly, the following specific aims are prioritized for this continuing research proposal: Aim I: Determine the in vivo biological significance of the genetic correlation of the renal-specific Na,K,2Cl-cotransporter gene with hypertension in Dahl S rats. Aim II: Determine the in vivo biological significance of the statistical interactive correlation of a1NK and NKC genes on salt-sensitive hypertension by developing dual transgenic (bigenic) Tg[Ra 1NK x nkc-F)] and Tg[Ra 1NK x nkc-A)] Dahl S rats. The successful completion of this research program will define a) the alNa,K-ATPase and the bumetanide-sensitive Na,K,2Cl-cotransporter as bona fide hypertension susceptibility genes in Dahl S rats; and b) will pave the way for the direct assessment of the role of these genes in hypertension susceptibility in different human populations. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE ARTERIOPATHY
OF
NOTCH3
SIGNALING
IN
HYPERTENSIVE
Principal Investigator & Institution: Pollman, Matthew J.; Medicine; Morehouse School of Medicine Atlanta, GA 30310 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 31-MAY-2007 Summary: (provided by applicant): The pathogenesis of hypertension-induced target organ damage is related to long-term changes in vessel function and structure determined by signaling pathways governing cell growth, programmed cell death, inflammation and matrix modulation. Within the spectrum of identified arteriopathies, CADASIL is a heritable syndrome of systemic small vessel disease predisposing to stroke and vascular dementia. The etiological basis for this syndrome is mutations within one of the Notch family of genes, Notch3. We have recently extended this clinical observation by studying hypertensive vessels and documenting the up-regulation of Notch3 expression in association with maladaptive vascular remodeling. Taken together, these clinical and animal model data support our central hypothesis that
Studies 63
Notch3 is a major determinant of vascular structure. Although it is well established that the vascular complications of hypertension are associated with pathological hypertrophy and matrix deposition, the molecular basis of this phenomenon remains poorly defined. Our preliminary data provides provocative new links between the pathology of hypertensive arteriopathy, the putative mediator TGF-beta1 and the Notch3 transcriptional pathway. The proposed project will test the central hypothesis that Notch3 signaling is a critical determinant of maladaptive hypertensive vascular remodeling by up-regulating a key downstream molecular mediator of VSMC hypertrophy and matrix production--TGF-beta1-through the activation of an RBP-Jkand HRT2-dependent transcriptional pathway. The hypothesis will be tested in vitro and in vivo by systematically implementing both a loss- and gain-of- function strategy, while addressing two fundamental questions: 1) What are the downstream determinants of hypertrophy and matrix production modulated by Notch3 in VSMC and 2) What is the biological significance of Notch3 signaling as a functional and structural determinant of maladaptive hypertensive vascular remodeling and target organ damage in vivo? Specifically, we will: Aim 1: Define the essential role of the Notch3RBP-Jk--HRT2 signaling pathway as a determinant of TGF-beta1 expression in cultured VSMC. Aim 2: Determine the functional role of a gain of Notch3 signaling in promoting maladaptive vascular remodeling and target organ damage in the context of secondary hypertension in Notch3 transgenic mice. Aim 3: Determine the essential mediator role of Notch3 signaling in promoting maladaptive hypertensive vascular remodeling and target organ damage in the context of secondary hypertension in Notch3 null mice. Aim 4: Determine the essential mediator role of Notch3 signaling in promoting maladaptive hypertensive vascular remodeling and target organ damage in the context of genetic hypertension in Notch3 null mice. The successful completion of the aims of this proposal are anticipated to provide novel mechanistic insights into the determinants of maladaptive vascular remodeling that may have important clinical implications for preventing hypertension-induced target organ damage. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF TGF-ALPHA IN PULMONARY VASCULAR DISEASE Principal Investigator & Institution: Le Cras, Timothy D.; Assistant Professor; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, OH 45229 Timing: Fiscal Year 2003; Project Start 10-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): Pulmonary hypertension plays a major role in the morbidity and mortality of a number of acute and chronic lung diseases including bronchopulmonary dysplasia. While clinical studies have implicated transforming growth factor-alpha (TGF-alpha) in the pathogenesis of these diseases, the role of TGFalpha, its cellular targets, and the signaling pathways involved are unclear. Preliminary data accompanying this application demonstrate that epithelial expression of TGF-alpha causes severe reductions in pulmonary artery number, vascular remodeling, and pulmonary hypertension as early as 2 weeks of age in transgenic mice. We also have preliminary evidence to suggest that this is mediated in part by autocrine signaling through EGF receptors on distal epithelial cells, and reductions in vascular endothelial growth factor-A (VEGF-A). Using both in vitro and in vivo approaches, this proposal will test the central hypothesis that epithelial expression of TGF-alpha disrupts vascular growth and causes vascular remodeling and pulmonary hypertension through EGF receptor-dependent autocrine-paracrine signaling. In the first phase we will define when pulmonary growth is disrupted by TGF-alpha, whether acute or chronic expression of TGF-alpha is necessary, and whether TGF-alpha causes vascular remodeling and
64 Hypertension
pulmonary hypertension independent of reductions in vascular growth (Specific Aim 1). In the second phase we will define the role of indirect signaling through the epithelium versus direct signaling to the vascular endothelium (Specific Aim 2) using a dominant negative (mutant) EGF receptor to block TGF-alpha signaling in specific cellular compartments. In the third phase we will define whether TGF-alpha, regulates expression of VEGF-A in type II epithelial cells in vitro and in vivo, and whether reductions in VEGF-A contribute to the pathogenesis of pulmonary vascular disease (Specific Aim 3). The overall goal of this proposal is to define the timing, cellular targets, and mechanism by which TGF-alpha disrupts pulmonary vascular growth and causes pulmonary hypertension and vascular remodeling. This information will serve as a basis for developing therapeutic strategies aimed at improving lung growth and preventing pulmonary hypertension in premature babies and adults. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF URIC ACID IN HYPERTENSION AND RENAL DISEASE Principal Investigator & Institution: Johnson, Richard; Associate Professor; Medicine; Baylor College of Medicine 1 Baylor Plaza Houston, TX 77030 Timing: Fiscal Year 2002; Project Start 01-JAN-2002; Project End 31-DEC-2006 Summary: (provided by applicant): The presence of an elevated serum uric acid is strongly associated with hypertension and renal disease. Despite the association and the ease with which to treat this condition, it remains unknown if the elevated uric acid has a pathogenic role in cardiovascular disease or whether it simply represents a 'marker' for other associated risk factors. Epidemiological studies have been unable to resolve this issue, and experimental studies have been thwarted by the absence of an animal model of mild hyperuricemia and by a paucity of cell culture studies. In preliminary data we have developed a model of mild hyperuricemia in rats and have found that they develop hypertension after several weeks through a crystal independent mechanism in which an afferent arteriolopathy develops in association with alterations in the renin angiotensin, cyclooxygenase-2 and nitric oxide pathways in the kidney. Mild hyperuricemia also results in interstitial renal disease, and hyperuricemia exacerbates renal injury in two different animal models. Our central hypothesis is that hyperuricemia induces hypertension and renal disease acutely by stimulating COX-2 in vascular smooth muscle cells and in the macula densa, which subsequently stimulates renin production, inhibits macula densa nitric oxide synthase, and raises blood pressure. Hyperuricemia also causes a primary afferent arteriolopathy that we hypothesize is mediated by local PDGF expression, and we postulate that once the arteriolopathy is established that salt-sensitive hypertension will persist even if the uric acid levels are corrected. In aim 1 we will examine the role of COX2 in our model, and will examine the kinetics of its expression and the effect of inhibition of COX2 on the alterations in renin, nitric oxide synthase, blood pressure and renal lesions. In aim 2 we will study the mechanism by which uric acid induces the arteriolopathy in our rats, and we will concentrate on the role of PDGF; furthermore, we will determine if the arteriolopathy provides a mechanism by which hypertension will be self-sustained despite correction of the hyperuricemia. In aim 3 we will initiate studies of the cellular mechanism by which uric acid stimulates PDGF and COX2 in cultured vascular smooth muscle cells and macula densa cells, with emphasis on the role of the recently cloned urate channel and on the MAP kinase cascade. Given that there are over 20 million individuals with hyperuricemia in the United States, and that 25-50% of all hypertensive individuals are hyperuricemic, we believe that studies examining the role of hyperuricemia in hypertension and cardiovascular disease are strongly indicated. We believe that the
Studies 65
preliminary data, coupled with the studies proposed, provide the first insights into a potential pathogenic mechanism by which uric acid induces hypertension and renal disease in rats, and may well provide important insights into the role of hyperuricemia in hypertension, cardiovascular and renal disease in man. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SCOR: MOLECULAR GENETICS OF HYPERTENSION Principal Investigator & Institution: Lifton, Richard P.; Chairman, Department of Genetics; Genetics; Yale University 47 College Street, Suite 203 New Haven, CT 065208047 Timing: Fiscal Year 2001; Project Start 01-FEB-1996; Project End 31-JAN-2006 Summary: The Yale Specialized Center of Research in Hypertension focuses on identification of the inherited abnormalities that contribute to high blood pressure and its consequences. To date, we have identified mutations in 4 genes that raise blood pressure, 8 genes that lower blood pressure, linkage for two more Mendelian hypertensive disease, and linkage for blood pressure in the general population. These findings have demonstrated the key role of renal salt homeostasis in determination of blood pressure variation in humans, and have begun to identify molecular mechanisms underlying relationships between blood pressure and bone density. In the current proposal, we propose a series of investigations that will extend these studies. Taking genes in which we have shown mutations alter blood pressure, we examine the impact of variants in these genes on blood pressure and related phenotypes in the Framingham Heart Study. We also search for a gene accounting for a substantial fraction of blood pressure variance in this population, and search for genes contributing to a common complication of hypertension, end stage renal disease. We continue our identification of Mendelian traits that affect blood pressure, and pursue the clinical consequences of these mutations. Finally, since virtually all known causes of hypertension act via a common pathway of increased activity of the amiloride-sensitive epithelial sodium channel, we investigate the signaling pathway that regulates the activity of this channel. These studies will continue to provide key information regarding the causes and consequences of hypertension in humans that have clinical and therapeutic implications. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: SCOR-MOLECULAR GENETICS OF HYPERTENSION Principal Investigator & Institution: Sigmund, Curt D.; Professor; Internal Medicine; University of Iowa Iowa City, IA 52242 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-JAN-2006 Summary: The application proposes to renew a Specialized Center of Research (SCOR) in the Molecular Genetics of Hypertension in the University of Iowa Cardiovascular Center. The overall theme is "Molecular and Physiologic Mechanisms of Genetic Hypertension in Humans and Experimental Animals." This initiative, which we have been planning for the past 18 months to fund 6 projects and one scientific core. The center brings together a cadre of investigators including outstanding molecular geneticists (Val Sheffield, Bento Soares and Curt Sigmund at Iowa and John Rapp in Ohio); molecular biologists (Peter Snyder and John Engelhardt); a genetic epidemiologist and biostatistician (Trudy Burns); and leading hypertension physiologists (Allyn Mark, John Stokes, Robin Davisson, Gerald DiBona, and Joseph Hill) to pursue the three broad goals of the Hypertension Molecular Genetics SCOR.
66 Hypertension
The strengths of the proposal include: (1) study of two distinctive human populations including nuclear families from the Muscatine population study of obesity and blood pressure; and Bedouin families from a homogenous population in Southern Israel with a high incidence of obesity; (2) a leading human and rat molecular genetics laboratory with capability for high throughput gene identification, sequencing of cDNAs, and generation and analysis of cDNA microarrays; (3) coordinated pursuit of chromosomal quantitative trait loci, physiologic and cellular intermediate phenotypes, and candidate genes in rat models of genetically salt-sensitive hypertension; (4) pursuit of functional data on the consequences of genetic variation in genes encoding the epithelial sodium channel; and (5) use of transgenic mice, tissue-specific knockout mice and mutant mouse strains to test the role of tissue-specific renin- angiotensin systems in hypertension and cardiac hypertrophy, and to study fundamental mechanisms in obesity-induced hypertension. These investigators have established vibrant collaborations within our SCOR and with investigators studying the genetics of hypertension at other institutions. This coalition of leading molecular geneticists and hypertension physiologists in the Iowa SCOR holds promise for continued substantial contribution to advancing knowledge of the molecular genetics of hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: STRUCTURE/FUNCTION OF THE MICROCIRCULATIOM Principal Investigator & Institution: Schmid-Schonbein, Geert W.; Professor; Applied Mechanics & Engr Scis; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, CA 92093 Timing: Fiscal Year 2001; Project Start 01-SEP-1978; Project End 31-MAR-2003 Summary: (Adapted from the application) The hypertensive syndrome is accompanied by a broad range of microvascular dysfunctions. The mechanisms responsible for development of cardiovascular complications in hypertension, however, have remained speculative. The applicant's hypothesis is that in addition to the definitive elevation of the blood pressure a key feature of hypertension is a shift in free radical formation at the tissue level which involves an adrenal/renal pathway. An oxidative stress on one hand leads to elevation of the arteriolar resistance while on the other hand it triggers a multitude of pathophysiological consequence, especially at the level of the microcirculation. Introduction of advanced microvascular techniques has enabled the investigators to identify higher levels of free radical production in-vivo in several models of hypertension together with a shift in the state of activation and interaction of cells in the circulation. The objective of this study is to investigate the mechanisms for the enhanced free radical production and outline its consequences for adjustments of microvascular function. In specific terms, the investigators propose to examine (I) the role of adrenal glucocorticoids and specific oxidases in free radical production, (II) mechanisms by which cell death, including apoptosis, are induced by oxidative stress relative to microvascular rarefaction (a loss of the smallest terminal arterioles and selected capillaries) and its modulation through the involvement of adrenal glucocorticoids, free radical production, and nitric oxide suppression, (III) the modification in the shear stress response of circulating leukocytes and endothelial cells in hypertensives as a consequence of glucocorticoids, and (IV) the basis for the reduced capacity of circulating leukocytes in hypertensives to respond to chemotactic stimuli, reduced adhesion to microvascular endothelium and the consequences for the migratory response. Several well-documented hypertensive models (spontaneously hypertensive rat, Dahl genetic salt-dependent hypertensive model, nitric oxide synthase gene knockout mouse) will be examined in a specific context in order to bring to light
Studies 67
common pathophysiological pathways which undermine the microcirculation in various forms of hypertension. Such a program will serve to clarify the pathogenesis of hypertension and is expected to stimulate the design of novel approaches for interventions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SYMPATHETIC NERVOUS SYSTEM REGULATION OF CELL ADHESION Principal Investigator & Institution: Mills, Paul J.; Professor; Psychiatry; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, CA 92093 Timing: Fiscal Year 2001; Project Start 01-AUG-1997; Project End 31-MAR-2005 Summary: Observations from the literature suggest that the SNS affects leukocyte endothelial interaction through at least four pathways: 1) circulating leukocyte cell adhesion molecule expression, particularly, increased CD11a expression; 2) elevated endothelial cell adhesion molecule expression (as indexed by elevated circulating levels of sCD54); 3) increased formation of leukocyte-platelet aggregates, which in turn enhance leukocyte adhesion to the endothelium; and 4) increased production of proinflammatory cytokines, particularly IL-6 and TNF-alpha, that in turn enhance the expression of leukocyte and endothelial cell adhesion molecules. The potential disease implications of these findings are not well understood. We have also gathered preliminary data suggesting that subjects with hypertension, as compared to subjects with normal blood pressure, exhibit exaggerated responses in each of these four pathways. Hypertensives show: 1) increased density of lymphocyte CD11a at rest and in response to stressors; 2) elevated resting and stressor-induced levels of circulating soluble sCD54; 3) increased SNS-induced formation of leukocyte-platelet aggregates in circulation; and 4) increased production of proinflammatory cytokines. This project will examine these pathways, particularly the effect of sCD54 on in vitro leukocyte adhesion in hypertension, the effects of platelet activation on leukocyte adhesion in hypertension, and the potential role of adhesion molecule-inducing proinflammatory cytokines on increased adhesion in hypertension. We propose to study 40 hypertensive and 40 normotensive women and men prior to and following an exhaustive exercise task and an infusion of the beta-adrenergic agonist isoproterenol. The overarching hypothesis of the proposal is that hypertension combined with sympathetic activation results in enhanced effects on leukocyte, platelet and endothelial adhesion that are of likely clinical significance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: TGF-BETA1, RENAL DISEASE AND HYPERTENSION Principal Investigator & Institution: August, Phyllis; Professor of Medicine; Medicine; Weill Medical College of Cornell Univ New York, NY 10021 Timing: Fiscal Year 2001; Project Start 01-JUN-2000; Project End 31-MAY-2005 Summary: Dr. Phyllis August's application for a K24 is based on her accomplishments as an investigator in patient oriented research, her significant track record of mentoring young investigators, and the research plan that explores an exciting new area of investigation in hypertension and renal disease in humans. Dr. August's past research has focused on hypertension and renal disease, especially hypertensive disorders in pregnancy. She has made original and significant discoveries with respect to regulation of blood pressure and calcium metabolism in normal and hypertensive pregnancy, and recently discovered that transforming growth factor-beta1 (TGF-beta1) is
68 Hypertension
hyperexpressed in hypertensives. Also, TGF- beta1 was hyperexpressed in Africa Americans with hypertension and/or renal disease compared to their Caucasian counterparts. The research proposed for this award explores the role of TGF-beta1 hyperexpression in the pathogenesis of renal disease and hypertension. The objective of this research is to test the hypothesis that hyperexpression of TGF-beta1, a multifunctional cytokine clearly shown to induce renal disease in experimental models, is a risk factor for the progression of renal disease to end stage renal disease (ESRD) in humans. That TGF-beta1 overexpression is more frequent in African Americans, a population at greater risk for ESRD than Caucasians, and that TGF-beta1 expression is determined by TGF-beta1 DNA polymorphisms will be explored in this study with conceptually interrelated clinical and laboratory studies. Dr. August will have the primary responsibility for these studies in the next 5 years. Studies suitable for beginning investigators to develop research careers are also proposed and include, 1) investigation of TGF-beta1 as a therapeutic target for angiotensin II receptor blockade, 2) characterization of placental cytokine gene expression profiles in normal and hypertensive pregnancy, 3) clinical studies of human renovascular hypertension. Further goals include obtaining additional training in research methodology, biostatistics, and genetic epidemiology. A long-term goal is to further develop the research program in hypertensive disorders of pregnancy by training young investigators. The resources and environment at Cornell including the laboratory expertise of Dr. Suthanthiran, the broad based patient population available via the Hypertension Center and by the applicant's joint appointment in Obstetrics, the established clinical research programs (including GCRC) together provide the necessary environment to conduct the proposed research and provide mentoring to new investigators. The K24 award will provide invaluable protected time for the development of the above research protocols, for obtaining new research skills, and for ensuring the mentoring of new investigators who will continue to conduct patient oriented research in the field of kidney disease, hypertension, and hypertension in pregnancy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE ANGIOTENSINOGEN GENE AND HUMAN HYPERTENSION Principal Investigator & Institution: Jorde, Lynn B.; Professor; Human Genetics; University of Utah 200 S University St Salt Lake City, UT 84112 Timing: Fiscal Year 2003; Project Start 27-JAN-2003; Project End 31-DEC-2006 Summary: (provided by applicant): Essential hypertension affects at least 25 percent of American adults, and it is a primary risk factor for heart failure, stroke, and kidney disease. Many, but not all, studies have shown that variants of the angiotensinogen gene (AGT) affect the risk of hypertension, but association studies conducted to date have been compromised by genetic heterogeneity and by the inherent complexity of hypertension as a phenotype. To overcome these difficulties, we will sequence or genotype a 14.4 kb region including AGT in more than 1,600 individuals sampled from populations throughout the world. This will permit us to explore fully the extent of allelic heterogeneity, haplotype variation, and potential for population stratification in the AGT gene. Approximately 600 of these individuals are clinically uncharacterized and will represent a broad range of worldwide human variation. Another 500 subjects are members of 40 Utah pedigrees that are part of the CEPH collection. These unique families have been heavily characterized genetically, and they are now being phenotyped for variables that include anthropometrics, blood chemistries, blood pressure measures, and plasma and urinary angiotensinogen. We will address the issue
Studies 69
of genetic heterogeneity by testing associations between multi-SNP AGT haplotypes, angiotensinogen levels, and blood pressure. In addition, linkage disequilibrium patterns will be assessed to determine the density and nature of SNPs best suited for localizing a gene underlying a complex trait. We will address the issue of phenotypic heterogeneity in hypertension by performing extensive SNP typing on a set of 400 hypertensives and 100 normotensives collected by Dr. Gordon Williams. These clinically well-characterized subjects have been tested for their response to infused angiotensin-II under high and low sodium intake. This direct probe provides a hypertension endophenotype that is closer to the function of the AGT gene, yielding a more realistic and informative assessment of the relationship between AGT haplotype variation and hypertension risk. A phylogenetic analysis of AGT sequence variation in our worldwide sample will help to assess population stratification in association studies. In addition, this sample will allow us to test the hypothesis that the ancestral T235 AGT allele provided a selective advantage in the sodium-poor environment of sub-Saharan Africa. The results of this analysis may help to explain why African-Americans have elevated rates of hypertension. In summary, our extensive analysis of AGT variation in more than 1,600 subjects will clarify the role of this gene in essential hypertension and will test specific hypotheses about the evolution of AGT. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TRANSGENIC STUDY VASCULAR ROLE OF NEUROPEPTIDE Y Principal Investigator & Institution: Michalkiewicz, Michael; Physiology; West Virginia University P. O. Box 6845 Morgantown, WV 265066845 Timing: Fiscal Year 2001; Project Start 15-DEC-1998; Project End 31-MAR-2001 Summary: Neuropeptide Y (NPY) with its multiple receptor subtypes is emerging as an important sympathetic regulator of cardiovascular and metabolic functions. Very potent vasoconstrictor and appetite stimulating activities of NPY suggest the physiological importance of this peptide and its involvement in the pathogenesis of hypertension and obesity. Antagonizing specific NPY activities may offer new avenues for treatment these diseases. This project tests the hypothesis that endogenous NPY by activating its own receptor increases vascular tone directly or indirectly by modulating adrenergic transmission to the blood vessels and that an increased chronic expression of the NPY gene will cause the development of hypertension. To test this hypothesis the NPY transgenic of Sprague Dawley rats were generated in which endogenous NPY is overexpressed under its natural promoter allowing for physiological regulation in the constitutive sites. These animals develop persistent hypertension with mildly elevated body weight. Using this model, the role of NPY and its newly discovered receptors in the long-term regulation of cardiovascular functions will be determined. Four Specific Aims are proposed: (1) Analyze the pattern of NPY overexpression at the protein and mRNA levels in the NPY transgenic male and female rats with particular emphasis on the constitutive sites of endogenous NPY production involved in the cardiovascular regulation; (2a) Determine the effect of NPY overexpression on arterial blood pressure and vascular resistance in male and female rats; and (2b) using available specific NPY receptor antagonists, identify the NPY receptor(s) involved in the development of the hypertension in the NPY transgenic rats; (3) Determine the effect of NPY overexpression on the adrenergic transmission to blood vessels by measuring a) pressor responsiveness to an adrenergic agonist norepinephrine (alpha1/alpha2); and b) (alpha1/ alpha2) responsiveness of the submandibular gland blood flow to supramaximal nerve stimulation; (4) Evaluate the contribution of increased food consumption and body weight to the development of the hypertension in the NPY
70 Hypertension
transgenic rats using a pair feeding approach. This studies will determine the role of endogenous NPY and its receptors in a long-term regulation of blood pressure and the mechanisms of the cooperation between the sympathetic neurotransmitters. The NPY overexpressing rats with well defined mutation of the NPY gene will provide a new transgenic animal model of hypertension; such a model should also be very useful for development of new therapies for treating this diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TREATMENT INTENSITIES
OF
HYPERTENSION
WITH
TWO
EXERCISE
Principal Investigator & Institution: Posner, Joel D.; Medicine; Mcp Hahnemann University Broad & Vine Sts Philadelphia, PA 19102 Timing: Fiscal Year 2001; Project Start 15-JUN-1997; Project End 31-MAY-2004 Summary: (Adapted from Investigator's Abstract) Arterial hypertension affects over 50 million Americans. While drug treatment is effective, exercise would be safer, might be cheaper, and would bring added health benefits if it could replace drugs in controlling hypertension. The aims of this study are to: 1) determine if two 18 month long endurance training programs, one of high intensity and one of moderate intensity, can replace medication as a treatment for mild essential hypertension, 2) determine if a moderate intensity endurance training program is as effective as or more effective than a high intensity program in allowing mild essential hypertensives to discontinue antihypertensive medication, 3) determine if physiological, psychological, and compliance variables predict success in allowing mild essential hypertensives to discontinue antihypertensive medication. The investigators propose a randomized controlled trial. Known hypertensives (n=162) whose diastolic blood pressures rises to between 90 and 104 within four months of discontinuing medication under careful observation will have their pressures controlled with enalapril. Half the subjects will be female and half male, and their racial characteristics will generally reflect that of our managed care population (about 20% black). V02 peak will be measured during cycle ergometry. Eligible subjects will be randomly assigned to 18 months participation in one of three groups: 1) high intensity endurance training (35 minutes 3 times/week at heart rate at 70-85% of V02 peak), 2) moderate intensity endurance training (35 minutes 3 times/week at heart rate of 50-70 of V02 peak), and 3) contact control. Enalapril will be forward or back titrated or discontinued to maintain a normal blood pressure. After 12 months participation, medication will be withdrawn under careful supervision from all subjects still taking it. They will test the hypotheses that: 1) a greater number of subjects undergoing either or both of the two 18 month exercise training programs will be able to stop antihypertensive medication than non-exercising controls, 2) moderate and high intensity endurance training are equally effective in replacing drugs in the treatment of mild essential hypertension, and 3) subjects that are successful at withdrawing antihypertensive medication will have: greater improvements in V02 peak, better initial psychological status or greater improvements in psychological status, and greater compliance with the exercise training program. The investigators state that this study will be a critical test of whether endurance training can replace medication in an important number of patients as a treatment for hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TULANE COBRE IN HYPERTENSION AND RENAL BIOLOGY Principal Investigator & Institution: Navar, L. Gabriel.; Professor and Chairman; Physiology; Tulane University of Louisiana New Orleans, LA 70118
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Timing: Fiscal Year 2002; Project Start 20-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): Hypertension is a leading cause of death and disability affecting 50 million people in the United States and responsible for 200,000 deaths annually. Because hypertension and associated cardiovascular diseases are particularly prevalent in Louisiana, Tulane Health Sciences Center established a Hypertension and Renal Center of Excellence, which consists of investigators in the School of Medicine and the School of Public Health and Tropical Medicine. The close linkage between hypertension and renal research is due to the growing recognition that many forms of hypertension result from abnormalities in kidney function due either to primary renal disease or to abnormal hormonal or environmental influences on the kidney that affect renal hemodynamics or tubular transport function. Disorders of sodium reabsorption by the renal tubules may lead to inadequate urinary excretion of salt, and derangements in vascular control mechanisms contribute to various forms of hypertension. Inappropriate activation of the renin-angiotensin system also leads to sodium retention and the development of hypertension with ensuing progressive renal and vascular injury. The objectives of this proposal are to provide an enriched mentoring environment to our junior faculty investigators so that they can achieve independent status and national competitiveness and to augment and strengthen biomedical research capacity at Tulane and the state of Louisiana in hypertension and associated renal and cardiovascular disease. The individual projects ranging from basic studies on development and function of the kidney to clinical and epidemiologic studies have been designed and will be performed by the junior faculty investigators who will be mentored by senior experienced faculty. Projects designated for initial support include investigations on the roles of angiotensin receptors in the control of the renal microvasculature and in kidney development and the roles of the newly described Heme-Heme oxygenase-carbon monoxide system and of cytochrome P450 metabolites in experimental and clinical hypertension. Epidemiologic studies will evaluate the effects of lifestyle modification (exercise) on hypertension in order to reduce blood pressure-related cardiovascular and renal disease in general but with emphasis on African-Americans. Accordingly, this COBRE will provide pivotal support needed to increase the number of competitive scientists in Louisiana in a disease specific area of extremely high biomedical relevance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: URIC ACID IN CHILDHOOD HYPERTENSION Principal Investigator & Institution: Feig, Daniel I.; Pediatrics; Baylor College of Medicine 1 Baylor Plaza Houston, TX 77030 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): An association between hyperuricemia and hypertension has been observed repeatedly since the 1870s. Generally the link was dismissed as having no causal role because of an assumption that the increase in serum uric acid was merely a surrogate for decreased glomerular filtration rate. Recently the association has been reevaluated because of results from several large clinical trials that implicate hyperuricemia as an independent risk factor for poor cardiovascular outcomes. Our own data demonstrates a close correlation between serum uric acid and primary hypertension in children. Furthermore, data from experiments using a model of mild hyperuricemia in rats reveal that the hyperuricemia alone is (1) sufficient to lead to hypertension and (2) exacerbates the progressive renal injury associated with either Cyclosporin A nephrotoxicity or surgical 5/6 nephrectomy. In the animal model, the mechanisms involved in these processes include uric acid mediated activation of
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cyclooxygenase-II, activation of the renin angiotensin system and down regulation of renal nitric oxide synthase. If these animal studies can be generalized to human populations, control of mild hyperuricemia will provide a new approach to management of hypertension as well as a novel therapeutic target for the prevention of progressive renal disease and cardiovascular morbidity. We propose to test whether the use of the xanthine oxidase inhibitor allopurinol, a uric acid lowering drug, will (1) ameliorate primary hypertension in children and (2) control hypertension in renal transplant recipients receiving cyclosporin or tacrolimus. We will further investigate the physiological mechanism by which serum uric acid levels are elevated in hypertensive children and the biochemical mechanisms by which elevated serum uric acid lead to increased blood pressure. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: VASCULAR CONSEQUENCES OF SYMPATHETIC NEURAL ACTIVATION IN OBESITY Principal Investigator & Institution: Haynes, William G.; Associate Professor; University of Iowa Iowa City, IA 52242 Timing: Fiscal Year 2003; Project Start 21-JAN-2003; Project End 31-DEC-2007 Summary: The mechanisms underlying the association between obesity and hypertension are unclear, but increased sympathetic neural drive to skeletal muscle circulation and kidney has been implicated. This insight has been derived from direct intraneural recordings of sympathetic nerve activity and regional norepinephrine turnover. It has been assumed that the increases in sympathetic nerve activity (SNA) directly translate into elevated sympathetic vasoconstrictor tone, but these assumptions have not been rigorously tested. We have recently obtained preliminary data using maximal alpha-adrenergic receptor blockade of the forearm vasculature that demonstrates no increase in sympathetic vascular tone in normotensive obese humans despite increased muscle SNA. This suggests that there is dissociation between sympathetic neural outflow and sympathetically mediated vasoconstrictor tone. Interestingly, we also have preliminary data indicating that in obese hypertensive humans, increased muscle SNA is associated with increased sympathetic vasoconstrictor tone. This suggests that a predisposition to hypertension interacts with obesity to permit the increased SNA to be expressed as increased sympathetic vascular tone. This project will test the hypothesis that the vasoconstrictor effects of SNA are attenuated in obesity but preserved in obese humans with a predisposition to hypertension, with these specific aims: 1) What are the effects of hypertension, obstructive sleep apnea and visceral adiposity on the resistance vessel expression of elevated SNA? 2) Is endothelial nitric oxide generation responsible for attenuated effects of SNA on vascular tone in obese compared to lean normotensive humans, and is the modulating influence of nitric oxide attenuated in obese hypertensive humans? 3) What are the effects of different dietary components on SNA and sympathetically mediated vasoconstrictor tone in obese normotensive and hypertensive subjects? Sympathetic nerve traffic to skin and skeletal muscle will be assessed by microneurography. Sympathetic vasoconstrictor tone will be assessed by the vasodilator response of skin (laser Doppler flux) and skeletal muscle (oxygenation measured by near infra-red oximetry) to intra-arterial infusion of an alpha-adrenergic antagonist. These studies should provide new insights into the cardiovascular effects of obesity and the factors that predispose to obesity-related hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: VASCULAR MODULATION
EXTRACELLULAR
SUPEROXIDE
DISMUTASE
Principal Investigator & Institution: Fukai, Tohru; Emory University 1784 North Decatur Road Atlanta, GA 30322 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: (provided by the applicant): Extracellular superoxide dismutase (ecSOD), a major form of SOD expressed in the vasculature, is a "secretory" copper-containing enzyme and plays an important role in regulating blood pressure and endothelial function by modulating the levels of O2 in the extracellular space. Particularly, in angiotensin H-induced hypertension model, the excessive 02 is observed in the vessel wall and the hypertension is ameliorated by treatment with membrane-targeted forms of SOD. Moreover, we have found that blood pressure and 02 production in the vessel were highly elevated in ecSOD-deficient mice infused with angiotensin II. Thus, ecS0D is a potentially important modulator of oxidative phenomena in the pathogenesis of hypertension. Recently, it has been shown that copper chaperones (CCS) are critical for copper transport and delivery to copper containing enzymes. Our preliminary data strongly suggests that CCS with signal peptide (CCS-SP) which targets to Golgi plays an important role in the transport of copper to ecSOD, which is required for full activity of the ecSOD. We will propose the following specific aim to address how ecSOD activity is controlled by copper transport system such as CCS and copper transporter in the yeast system, vascular cells and in vivo model of hypertension. In aim 1, we will characterize a role of copper transport system for full expression of ecSOD activity using the yeast system. First, by generating several CCS-SP cDNA constructs including the truncated form, we will determine which region is critical for copper loading-to ecSOD. Second, we will determine if copper loading to ecSOD requires MNK, a copper transporter in the trans-Golgi network, using the yeast strain deficient in MNK. In aim 2, we will identify endogenous copper chaperone for ecSOD in human aortic smooth muscle cells (HASM) that highly expresses ecSOD, by using the highly conserved region of CCS as a probe that have detected novel CCS-like transcript and protein in HASM. Next, we will determine if copper delivery to ecSOD requires MTNK in mammalian cells, by using the murine MNK-mutant fibroblast and aorta from MNK-mutant mice. In aim 3, we will examine the role of copper transport system for ecSOD in blood pressure, vascular O2 production and endothelial function in angiotensin II induced hypertension by using MNK-mutant mice. These studies will provide new insight into a copper transport system for ecSOD as a novel modulator of oxidative stress linked to the pathogenesis of hypertension and as essential to anti-oxidant therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and
3 4
Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age.
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unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “hypertension” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for hypertension in the PubMed Central database: •
[beta]-Blockers as first-line therapy for hypertension. by Heckman GA, Papaioannou A, Parkinson W, Patterson CA. 2000 Nov 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=80403
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A De novo Missense Mutation of the [beta] Subunit of the Epithelial Sodium Channel Causes Hypertension and Liddle Syndrome, Identifying a Proline-Rich Segment Critical for Regulation of Channel Activity. by Hansson JH, Schild L, Lu Y, Wilson TA, Gautschi I, Shimkets R, Nelson-Williams C, Rossier BC, Lifton RP. 1995 Dec 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=40428
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A genetic defect resulting in mild low-renin hypertension. by Wilson RC, DaveSharma S, Wei JQ, Obeyesekere VR, Li K, Ferrari P, Krozowski ZS, Shackleton CH, Bradlow L, Wiens T, New MI. 1998 Aug 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=21485
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A genetically clamped renin transgene for the induction of hypertension. by Caron KM, James LR, Kim HS, Morham SG, Lopez ML, Gomez RA, Reudelhuber TL, Smithies O. 2002 Jun 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123053
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A new era in hypertension research: discussing the findings of ALLHAT. by Furberg CD. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=64822
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A Review of the Adverse Effects of Peripheral Alpha-1 Antagonists in Hypertension Therapy. by Bryson CL MD, Psaty BM MD PhD. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=134479
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Activation of the Fas/Fas ligand pathway in hypertensive renal disease in Dahl/Rapp rats. by Sanders PW, Wang PX. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=64784
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Acute hemodynamic effects of inhaled nitric oxide, dobutamine and a combination of the two in patients with mild to moderate secondary pulmonary hypertension. by Vizza CD, Rocca GD, Roma DA, Iacoboni C, Pierconti F, Venuta F, Rendina E, Schmid G, Pietropaoli P, Fedele F. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=96124
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Acute visual loss after initiation of antihypertensive therapy: case report. by Mainville N, Connolly WE. 2003 Aug 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=180657
5
The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.
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Adipocyte-derived leucine aminopeptidase genotype and response to antihypertensive therapy. by Hallberg P, Lind L, Michaelsson K, Kurland L, Kahan T, Malmqvist K, Ohman KP, Nystrom F, Liljedahl U, Syvanen AC, Melhus H. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=212555
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Alterations in the regulation of androgen-sensitive Cyp 4a monooxygenases cause hypertension. by Holla VR, Adas F, Imig JD, Zhao X, Price E Jr, Olsen N, Kovacs WJ, Magnuson MA, Keeney DS, Breyer MD, Falck JR, Waterman MR, Capdevila JH. 2001 Apr 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=33189
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Aminopeptidase A inhibitors as potential central antihypertensive agents. by Reaux A, Fournie-Zaluski MC, David C, Zini S, Roques BP, Corvol P, Llorens-Cortes C. 1999 Nov 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23962
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Anorexigen-induced pulmonary hypertension and the serotonin (5-HT) hypothesis: lessons for the future in pathogenesis. by Eddahibi S, Adnot S. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=64820
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Arterial expression of 5-HT2B and 5-HT1B receptors during development of DOCAsalt hypertension. by Banes AK, Watts SW. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=201025
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Atherosclerotic ischemic renal disease. Diagnosis and prevalence in an hypertensive and/or uremic elderly population. by Coen G, Calabria S, Lai S, Moscaritolo E, Nofroni I, Ronga G, Rossi M, Ventroni G, Sardella D, Ferrannini M, Zaccaria A, Cianci R. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=150566
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Benign intracranial hypertension secondary to nasal fluticasone propionate. by Bond DW, Charlton CP. 2001 Apr 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=30587
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Bone morphogenetic proteins, genetics and the pathophysiology of primary pulmonary hypertension. by Caestecker MD, Meyrick B. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=59576
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Cardiovascular Effects of Fermented Milk Containing Angiotensin-Converting Enzyme Inhibitors Evaluated in Permanently Catheterized, Spontaneously Hypertensive Rats. by Fuglsang A, Nilsson D, Nyborg NC. 2002 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=126801
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Changes in left ventricular structure and function in patients with white coat hypertension: cross sectional survey. by Muscholl MW, Hense HW, Brockel U, Doring A, Riegger GA, Schunkert H. 1998 Aug 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28649
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Chronic Control of High Blood Pressure in the Spontaneously Hypertensive Rat by Delivery of Angiotensin Type 1 Receptor Antisense. by Iyer SN, Lu D, Katovich MJ, Raizada MK. 1996 Sep 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=38537
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Clinical Trials in Hypertension. by Springer AJ. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=101190
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Combination treatment effective option for hypertensive, diabetic patients with microalbuminuria. by Chen BH. 2001 Mar 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=80906
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Conditional and targeted overexpression of vascular chymase causes hypertension in transgenic mice. by Ju H, Gros R, You X, Tsang S, Husain M, Rabinovitch M. 2001 Jun 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=34692
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Correction of Hypertension by Normalization of Endothelial Levels of Fibroblast Growth Factor and Nitric Oxide Synthase in Spontaneously Hypertensive Rats. by Cuevas P, Garcia-Calvo M, Carceller F, Reimers D, Zazo M, Cuevas B, Munoz-Willery I, Martinez-Coso V, Lamas S, Gimenez-Gallego G. 1996 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=38172
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Cost effectiveness analysis of improved blood pressure control in hypertensive patients with type 2 diabetes: UKPDS 40. by [No authors listed]; 1998 Sep 12; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28661
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Cyclosporine A-induced hypertension involves synapsin in renal sensory nerve endings. by Zhang W, Li JL, Hosaka M, Janz R, Shelton JM, Albright GM, Richardson JA, Sudhof TC, Victor RG. 2000 Aug 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16939
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Defective G Protein Activation of the cAMP Pathway in Rat Kidney During Genetic Hypertension. by Chatziantoniou C, Ruan X, Arendshorst WJ. 1995 Mar 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=42331
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Defects in caveolin-1 cause dilated cardiomyopathy and pulmonary hypertension in knockout mice. by Zhao YY, Liu Y, Stan RV, Fan L, Gu Y, Dalton N, Chu PH, Peterson K, Ross J Jr, Chien KR. 2002 Aug 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123264
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Delivery of Angiotensin II Type 1 Receptor Antisense Inhibits Angiotensin Action in Neurons from Hypertensive Rat Brain. by Lu D, Raizada MK. 1995 Mar 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=42329
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Dissection of a Quantitative Trait Locus for Genetic Hypertension on Rat Chromosome 10. by Kreutz R, Hubner N, James MR, Bihoreau M, Gauguier D, Lathrop GM, Ganten D, Lindpaintner K. 1995 Sep 12; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41050
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Diuretics: again the first step in the treatment of most patients with hypertension. by Fuchs FD. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=59527
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Do hypertensive patients with average cholesterol levels benefit from atorvastatin therapy? by Hackam DG. 2003 Jun 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=161615
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Does Superoxide Underlie the Pathogenesis of Hypertension? by Nakazono K, Watanabe N, Matsuno K, Sasaki J, Sato T, Inoue M. 1991 Nov 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52864
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Down-regulation of the expression of endothelial NO synthase is likely to contribute to glucocorticoid-mediated hypertension. by Wallerath T, Witte K, Schafer SC, Schwarz PM, Prellwitz W, Wohlfart P, Kleinert H, Lehr HA, Lemmer B, Forstermann U. 1999 Nov 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23952
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Dual Inhibition of Angiotensin-Converting Enzyme and Neutral Endopeptidase by the Orally Active Inhibitor Mixanpril: A Potential Therapeutic Approach in Hypertension. by Fournie-Zaluski MC, Gonzalez W, Turcaud S, Pham I, Roques BP, Michel JB. 1994 Apr 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=43725
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Effect of Increasing Doses of Angiotensin II Infused into Normal and Hypertensive Wistar Rats on Low Density Lipoprotein and Fibrinogen Uptake by Aortic Walls. by Cardon-Sanclemente LE, Medina R, Born GV. 1994 Apr 12; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=43561
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Endogenous Biosynthesis of Arachidonic Acid Epoxides in Humans: Increased Formation in Pregnancy-Induced Hypertension. by Catella F, Lawson JA, Fitzgerald DJ, FitzGerald GA. 1990 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54435
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Episodic coronary artery vasospasm and hypertension develop in the absence of Sur2 KATP channels. by Chutkow WA, Pu J, Wheeler MT, Wada T, Makielski JC, Burant CF, McNally EM. 2002 Jul 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151064
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Evaluation of computer based clinical decision support system and risk chart for management of hypertension in primary care: randomised controlled trial. by Montgomery AA, Fahey T, Peters TJ, MacIntosh C, Sharp DJ. 2000 Mar 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27312
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Evidential hypertension. by Wright JM. 2002 Jan 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=99235
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Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. by Maynard SE, Min JY, Merchan J, Lim KH, Li J, Mondal S, Libermann TA, Morgan JP, Sellke FW, Stillman IE, Epstein FH, Sukhatme VP, Karumanchi SA. 2003 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151901
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First-line drugs for hypertension. by Spence JD. 2001 Jan 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=80672
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First-line drugs for hypertension. by Wright JM. 2001 Jan 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=80673
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Functional Heterogeneity of Bone Morphogenetic Protein Receptor-II Mutants Found in Patients with Primary Pulmonary Hypertension. by Nishihara A, Watabe T, Imamura T, Miyazono K. 2002 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=124142
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G protein-coupled receptor kinase 4 gene variants in human essential hypertension. by Felder RA, Sanada H, Xu J, Yu PY, Wang Z, Watanabe H, Asico LD, Wang W, Zheng S, Yamaguchi I, Williams SM, Gainer J, Brown NJ, Hazen-Martin D, Wong LJ, Robillard JE, Carey RM, Eisner GM, Jose PA. 2002 Mar 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=122616
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Gene Targeting Approaches to Complex Genetic Diseases: Atherosclerosis and Essential Hypertension. by Smithies O, Maeda N. 1995 Jun 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41675
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Generalizability of guidelines and physicians' adherence. Case study on the Sixth Joint National Commitee's guidelines on hypertension. by Pedone C, Lapane KL. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=183849
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Genetic Determinants of Human Hypertension. by Lifton RP. 1995 Sep 12; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41004
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Genetic disruption of [gamma]-melanocyte --stimulating hormone signaling leads to salt-sensitive hypertension in the mouse. by Ni XP, Pearce D, Butler AA, Cone RD, Humphreys MH. 2003 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152936
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Genetically determined chloride-sensitive hypertension and stroke. by Tanaka M, Schmidlin O, Yi SL, Bollen AW, Morris RC Jr. 1997 Dec 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=25108
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Genomic approaches to research in pulmonary hypertension. by Geraci MW, Gao B, Hoshikawa Y, Yeager ME, Tuder RM, Voelkel NF. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=59578
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Heterozygous deficiency of hypoxia-inducible factor --2[alpha] protects mice against pulmonary hypertension and right ventricular dysfunction during prolonged hypoxia. by Brusselmans K, Compernolle V, Tjwa M, Wiesener MS, Maxwell PH, Collen D, Carmeliet P. 2003 May 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=155039
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How well can blood pressure be controlled? Progress report on the Systolic Hypertension in Europe Follow-Up Study (Syst-Eur 2). by Thijs L, Staessen JA, Beleva S, Birkenhager WH, Bulpitt CJ, Celis H, Fletcher AE, Kermova R, Leonetti G, Laks T, Mantov S, Nachev C, Sarti C, Tuomilehto J, Fagard RH. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=64833
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Hypertension and [alpha]-adrenergic blockers: preliminary ALLHAT results. by Chen BH. 2000 Aug 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=80393
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Hypertension and prolonged vasoconstrictor signaling in RGS2-deficient mice. by Heximer SP, Knutsen RH, Sun X, Kaltenbronn KM, Rhee MH, Peng N, Oliveira-dosSantos A, Penninger JM, Muslin AJ, Steinberg TH, Wyss JM, Mecham RP, Blumer KJ. 2003 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151918
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Hypertension in the Parsi community of Bombay: a study on prevalence, awareness and compliance to treatment. by Bharucha NE, Kuruvilla T. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=140316
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Hypertension, cardiac hypertrophy, and sudden death in mice lacking natriuretic peptide receptor A. by Oliver PM, Fox JE, Kim R, Rockman HA, Kim HS, Reddick RL, Pandey KN, Milgram SL, Smithies O, Maeda N. 1997 Dec 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=25105
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Hypertension: [beta] testing. by Kotlikoff M, Hall I. 2003 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=182214
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Hypertensive diseases of pregnancy and risk of hypertension and stroke in later life: results from cohort study. by Wilson BJ, Watson MS, Prescott GJ, Sunderland S, Campbell DM, Hannaford P, Smith WC. 2003 Apr 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153466
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Implications of recent hypertension trials for the generalist physician: whom do we treat, and how? by Green L. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=59591
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Increase in blood glucose concentration during antihypertensive treatment as a predictor of myocardial infarction: population based cohort study. by Dunder K, Lind L, Zethelius B, Berglund L, Lithell H. 2003 Mar 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152364
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Inhaled nitric oxide in persistent pulmonary hypertension of the newborn refractory to high-frequency ventilation. by Al-Alaiyan S, Neiley E. 1999; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=29006
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Inhaled nitric oxide reverses cell-free hemoglobin-induced pulmonary hypertension and decreased lung compliance. Preliminary results. by Figueiredo LF, Mathru M, Jones JR, Solanki D, Kramer GC. 1997; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28996
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Inverse Changes in Erythroid Cell Volume and Number Regulate the Hematocrit in Newborn Genetically Hypertensive Rats. by Boylan JW, Liew JB, Feig PU. 1991 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52818
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Low NO bioavailability in CCl4 cirrhotic rat livers might result from low NO synthesis combined with decreased superoxide dismutase activity allowing superoxide-mediated NO breakdown: A comparison of two portal hypertensive rat models with healthy controls. by Van de Casteele M, van Pelt JF, Nevens F, Fevery J, Reichen J. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=155038
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Modulation of the molecular composition of large conductance, Ca2 + activated K + channels in vascular smooth muscle during hypertension. by Amberg GC, Bonev AD, Rossow CF, Nelson MT, Santana LF. 2003 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=182211
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Mutations in the CYP11B1 Gene Causing Congenital Adrenal Hyperplasia and Hypertension Cluster in Exons 6, 7, and 8. by Curnow KM, Slutsker L, Vitek J, Cole T, Speiser PW, New MI, White PC, Pascoe L. 1993 May 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46550
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NCX-1000, a NO-releasing derivative of ursodeoxycholic acid, selectively delivers NO to the liver and protects against development of portal hypertension. by Fiorucci S, Antonelli E, Morelli O, Mencarelli A, Casini A, Mello T, Palazzetti B, Tallet D, del Soldato P, Morelli A. 2001 Jul 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=37532
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Negative regulators of sodium transport in the kidney: Key factors in understanding salt-sensitive hypertension? by Rossier BC. 2003 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152592
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Newly diagnosed hypertension. by A'Court C. 2002 Jun 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=115217
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Non-dipper treated hypertensive patients do not have increased cardiac structural alterations. by Cuspidi C, Michev I, Meani S, Valerio C, Bertazzoli G, Magrini F, Zanchetti A. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153424
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Nonlinear indicial response of complex nonstationary oscillations as pulmonary hypertension responding to step hypoxia. by Huang W, Shen Z, Huang NE, Fung YC. 1999 Mar 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26697
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Nonnarcotic analgesic use and the risk of hypertension. by O'Brien BD. 2003 May 27; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=155965
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Obesity drug sibutramine (Meridia): hypertension and cardiac arrhythmias. by Wooltorton E. 2002 May 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=111085
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Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study. by Lavie P, Herer P, Hoffstein V. 2000 Feb 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27290
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Omapatrilat normalizes renal function curve in spontaneously hypertensive rats. by Morazo P, Fortepiani LA, Clara Ortiz M, Atucha NM, Garcia-Estan J. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=57752
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Orlistat associated with hypertension. by Persson M, Vitols S. 2000 Jul 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27428
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Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension. by Landmesser U, Dikalov S, Price SR, McCann L, Fukai T, Holland SM, Mitch WE, Harrison DG. 2003 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152929
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Patients' decisions about whether or not to take antihypertensive drugs: qualitative study. by Benson J, Britten N. 2002 Oct 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129637
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Patients' views about taking antihypertensive drugs: questionnaire study. by Benson J, Britten N. 2003 Jun 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=161632
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Phenylpropanolamine, stroke and hypertension. by Kuchel O. 2001 Mar 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=80813
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Predictors of normotension on withdrawal of antihypertensive drugs in elderly patients: prospective study in second Australian national blood pressure study cohort. by Nelson MR, Reid CM, Krum H, Muir T, Ryan P, McNeil JJ. 2002 Oct 12; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128950
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Prevention of renovascular and cardiac pathophysiological changes in hypertension by angiotensin II type 1 receptor antisense gene therapy. by Martens JR, Reaves PY, Lu D, Katovich MJ, Berecek KH, Bishop SP, Raizada MK, Gelband CH. 1998 Mar 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19454
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Pulmonary Hypertension Syndrome in Broilers Caused by Enterococcus faecalis. by Tankson JD, Thaxton JP, Vizzier-Thaxton Y. 2001 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=98767
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Purification of Parathyroid Hypertensive Factor from Plasma of Spontaneously Hypertensive Rats. by Benishin CG, Lewanczuk RZ, Pang PK. 1991 Jul 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52085
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Randomised controlled trial of dual blockade of renin-angiotensin system in patients with hypertension, microalbuminuria, and non-insulin dependent diabetes: the candesartan and lisinopril microalbuminuria (CALM) study. by Mogensen CE, Neldam S, Tikkanen I, Oren S, Viskoper R, Watts RW, Cooper ME. 2000 Dec 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27545
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Rational Prescribing in Primary Care (RaPP-trial). A randomised trial of a tailored intervention to improve prescribing of antihypertensive and cholesterol-lowering drugs in general practice [ISRCTN48751230]. by Fretheim A, Oxman AD, Treweek S, Bjorndal A. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152643
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Relation between insufficient response to antihypertensive treatment and poor compliance with treatment: a prospective case-control study. by Nuesch R, Schroeder K, Dieterle T, Martina B, Battegay E. 2001 Jul 21; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=34727
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RGS2: a "turn-off" in hypertension. by Le TH, Coffman TM. 2003 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151929
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Salt-sensitive hypertension: if only it were as simple as rocket science. by Reudelhuber TL. 2003 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152948
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Should hypertension be treated with angiotensin-converting-enzyme inhibitors, calcium-channel blockers or diuretics? by Myers KA. 2003 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=151997
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Spontaneously hypertensive rats: further evaluation of age-related memory performance and cholinergic marker expression. by Hernandez CM, Hoifodt H, Terry AV Jr. 2003 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=161744
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Survival in treated hypertension: follow up study after two decades. by Andersson OK, Almgren T, Persson B, Samuelsson O, Hedner T, Wilhelmsen L. 1998 Jul 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28606
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The 2001 Canadian hypertension recommendations: take-home messages. by Campbell NR, Drouin D, Feldman RD. 2002 Sep 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=122031
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The management of hypertension in Canada: a review of current guidelines, their shortcomings and implications for the future. by McAlister FA, Campbell NR, Zarnke K, Levine M, Graham ID. 2001 Feb 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=80782
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The potential savings of using thiazides as the first choice antihypertensive drug: cost-minimisation analysis. by Fretheim A, Aaserud M, Oxman AD. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=201005
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The rat STSL locus: characterization, chromosomal assignment, and genetic variations in sitosterolemic hypertensive rats. by Yu H, Pandit B, Klett E, Lee MH, Lu K, Helou K, Ikeda I, Egashira N, Sato M, Klein R, Batta A, Salen G, Patel SB. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165443
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The value of industry-sponsored studies of initial antihypertensive therapies. by Caro JJ, Payne K. 2001 Jun 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=81187
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Thresholds for taking antihypertensive drugs in different professional and lay groups: questionnaire survey. by Steel N. 2000 May 27; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27388
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Transforming growth factor-[beta]1 hyperexpression in African-American hypertensives: A novel mediator of hypertension and /or target organ damage. by Suthanthiran M, Li B, Song JO, Ding R, Sharma VK, Schwartz JE, August P. 2000 Mar 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16265
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Upregulation of nitric oxide synthase in mice with severe hypoxia-induced pulmonary hypertension. by Fagan KA, Morrissey B, Fouty BW, Sato K, Harral JW, Morris KG Jr, Hoedt-Miller M, Vidmar S, McMurtry IF, Rodman DM. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=59521
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Up-Regulation of Pressure-activated Ca2+-permeable Cation Channel in Intact Vascular Endothelium of Hypertensive Rats. by Hoyer J, Kohler R, Haase W, Distler A. 1996 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=38316
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Use of antihypertensive medications in pregnancy and the risk of adverse perinatal outcomes: McMaster Outcome Study of Hypertension In Pregnancy 2 (MOS HIP 2). by Ray JG, Vermeulen MJ, Burrows EA, Burrows RF. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=60658
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Using thresholds based on risk of cardiovascular disease to target treatment for hypertension: modelling events averted and number treated. by Baker S, Priest P, Jackson R. 2000 Mar 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27311
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Vaccination for protection of retinal ganglion cells against death from glutamate cytotoxicity and ocular hypertension: Implications for glaucoma. by Schori H, Kipnis J, Yoles E, WoldeMussie E, Ruiz G, Wheeler LA, Schwartz M. 2001 Mar 13; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=30665
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Validation of Heart Failure Events in the Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) Participants Assigned to Doxazosin and Chlorthalidone. by Piller LB, Davis BR, Cutler JA, Cushman WC, Wright JT Jr, Williamson JD, Leenen FH, Einhorn PT, Randall OS, Golden JS, Haywood LJ. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=149403
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Vasoactive intestinal peptide as a new drug for treatment of primary pulmonary hypertension. by Petkov V, Mosgoeller W, Ziesche R, Raderer M, Stiebellehner L, Vonbank K, Funk GC, Hamilton G, Novotny C, Burian B, Block LH. 2003 May 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=154449
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When should hypertension be treated? The different perspectives of Canadian family physicians and patients. by McAlister FA, O'Connor AM, Wells G, Grover SA, Laupacis A. 2000 Aug 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=80373
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Xanthine oxidase activity associated with arterial blood pressure in spontaneously hypertensive rats. by Suzuki H, DeLano FA, Parks DA, Jamshidi N, Granger DN, Ishii H, Suematsu M, Zweifach BW, Schmid-Schonbein GW. 1998 Apr 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22563
The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with hypertension, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “hypertension” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for hypertension (hyperlinks lead to article summaries):
PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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A 25-year clinical history of portopulmonary hypertension associated with latent myeloproliferative disorder. Author(s): Ito H, Adachi Y, Arimura Y, Endo T, Hinoda Y, Imai K. Source: Journal of Gastroenterology. 2003; 38(5): 488-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12768393&dopt=Abstract
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A descriptive analysis of hypertension and affiliated therapies in a military retiree population (ages 40-85 years) at Camp Lejeune, North Carolina. Author(s): Johnson BW, Davies WG, Hardy DW, Varga J, Gallagher KL, Ryan MT, Jones RM. Source: Military Medicine. 2003 May; 168(5): 424-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775183&dopt=Abstract
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A meta-analysis of the effects of treatment on left ventricular mass in essential hypertension. Author(s): Klingbeil AU, Schneider M, Martus P, Messerli FH, Schmieder RE. Source: The American Journal of Medicine. 2003 July; 115(1): 41-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12867233&dopt=Abstract
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A model analysis of costs of blood pressure destabilization and edema associated with rofecoxib and celecoxib among older patients with osteoarthritis and hypertension in a Medicare Choice population. Author(s): Becker RV, Burke TA, McCoy MA, Trotter JP. Source: Clinical Therapeutics. 2003 February; 25(2): 647-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12749519&dopt=Abstract
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A novel mechanism for pulmonary arterial hypertension? Author(s): Cooke JP. Source: Circulation. 2003 September 23; 108(12): 1420-1. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14504250&dopt=Abstract
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A nurse-led initiative to screen and treat hypertension. Author(s): Terry J. Source: Community Nurse. 2000 May; 6(4): 23-4. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12778519&dopt=Abstract
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A simple case of hypertension? Author(s): Nageh T, Swann AD, Walker DM. Source: The British Journal of General Practice : the Journal of the Royal College of General Practitioners. 2003 May; 53(490): 392-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830568&dopt=Abstract
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A six-month randomized clinical trial comparing the IOP-lowering efficacy of bimatoprost and latanoprost in patients with ocular hypertension or glaucoma. Author(s): Robin AL. Source: American Journal of Ophthalmology. 2003 June; 135(6): 921-2; Author Reply 9223. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788149&dopt=Abstract
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A study of hepatopulmonary syndrome among patients of cirrhosis of liver and portal hypertension. Author(s): Hira HS, Kumar J, Tyagi SK, Jain SK. Source: Indian J Chest Dis Allied Sci. 2003 July-September; 45(3): 165-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12866633&dopt=Abstract
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Abdominal adiposity, age, education level and therapy associated with uncontrolled hypertension. Author(s): de Resende SM, Velasquez-Melendez G. Source: Journal of Human Hypertension. 2003 May; 17(5): 365-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756411&dopt=Abstract
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Acarbose treatment and the risk of cardiovascular disease and hypertension in patients with impaired glucose tolerance: the STOP-NIDDM trial. Author(s): Chiasson JL, Josse RG, Gomis R, Hanefeld M, Karasik A, Laakso M; STOPNIDDM Trial Research Group. Source: Jama : the Journal of the American Medical Association. 2003 July 23; 290(4): 486-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12876091&dopt=Abstract
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Acetaminophen and hypertension: a causal association or pain mediated? Author(s): Brotman DJ. Source: Archives of Internal Medicine. 2003 May 12; 163(9): 1113-4; Author Reply 1115-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742815&dopt=Abstract
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Acute endothelin A receptor antagonism improves pulmonary and systemic haemodynamics in patients with pulmonary arterial hypertension that is primary or autoimmune and related to congenital heart disease. Author(s): Apostolopoulou SC, Rammos S, Kyriakides ZS, Webb DJ, Johnston NR, Cokkinos DV, Kremastinos DT. Source: Heart (British Cardiac Society). 2003 October; 89(10): 1221-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12975426&dopt=Abstract
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Acute hemodynamic effects and home therapy using a novel pulsed nasal nitric oxide delivery system in children and young adults with pulmonary hypertension. Author(s): Ivy DD, Parker D, Doran A, Parker D, Kinsella JP, Abman SH. Source: The American Journal of Cardiology. 2003 October 1; 92(7): 886-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14516902&dopt=Abstract
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Acute intermittent porphyria: an unusual cause of malignant hypertension. Author(s): Singh V, Sud K, Kohli HS, Gupta KL, Sakhuja V. Source: J Assoc Physicians India. 2003 February; 51: 225-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12725276&dopt=Abstract
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Acute renal failure due to hypertension: malignant hypertension in an adolescent. Author(s): Tanaka H, Tateyama T, Suzuki K, Nakahata T, Kudo M, Takahashi Y, Ito E, Waga S. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 2003 June; 45(3): 342-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828593&dopt=Abstract
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Aeolus myth: chronic obstructive lung disease and nocturnal lumbosacral pain in association with lumbar spinal stenosis and pulmonary hypertension. Author(s): LaBan MM, Kucway EJ. Source: American Journal of Physical Medicine & Rehabilitation / Association of Academic Physiatrists. 2003 September; 82(9): 660-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12960906&dopt=Abstract
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Aldosterone antagonism and hypertension. Author(s): Conti CR. Source: Clin Cardiol. 2003 May; 26(5): 209-10. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769246&dopt=Abstract
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Ambulatory blood pressure measurement is now indispensable to the good clinical management of hypertension. Author(s): O'Brien E. Source: Cardiovasc J S Afr. 2003 May-June; 14(3): 113-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12844194&dopt=Abstract
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Analgesics and hypertension: causality or correlation? Author(s): Glaser JH. Source: Archives of Internal Medicine. 2003 May 12; 163(9): 1114; Author Reply 1115-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742817&dopt=Abstract
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Angiopoietin-1 and pulmonary hypertension: cause or cure? Author(s): Rudge JS, Thurston G, Yancopoulos GD. Source: Circulation Research. 2003 May 16; 92(9): 947-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750304&dopt=Abstract
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Angiotensin-converting-enzyme inhibitors and diuretics for hypertension. Author(s): Esnault VL. Source: The New England Journal of Medicine. 2003 July 3; 349(1): 90-3; Author Reply 90-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846229&dopt=Abstract
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Angiotensin-converting-enzyme inhibitors and diuretics for hypertension. Author(s): Reese AM, Talbert RL, Bussey HI. Source: The New England Journal of Medicine. 2003 July 3; 349(1): 90-3; Author Reply 90-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846228&dopt=Abstract
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Angiotensin-converting-enzyme inhibitors and diuretics for hypertension. Author(s): Krut LH. Source: The New England Journal of Medicine. 2003 July 3; 349(1): 90-3; Author Reply 90-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846227&dopt=Abstract
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Angiotensin-converting-enzyme inhibitors and diuretics for hypertension. Author(s): Davis BR, Wright JT Jr, Cutler JA. Source: The New England Journal of Medicine. 2003 July 3; 349(1): 90-3; Author Reply 90-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846226&dopt=Abstract
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Angiotensin-converting-enzyme inhibitors and diuretics for hypertension. Author(s): Pickering TG. Source: The New England Journal of Medicine. 2003 July 3; 349(1): 90-3; Author Reply 90-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840099&dopt=Abstract
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Angiotensinogen and angiotensin II type 1 receptor gene polymorphism in patients with autosomal dominant polycystic kidney disease: effect on hypertension and ESRD. Author(s): Lee KB, Kim UK. Source: Yonsei Medical Journal. 2003 August 30; 44(4): 641-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950120&dopt=Abstract
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Antibiotics in primary prevention of myocardial infarction among elderly patients with hypertension. Author(s): Brassard P, Bourgault C, Brophy J, Kezouh A, Rainville B, Xhignesse M, Suissa S. Source: American Heart Journal. 2003 May; 145(5): E20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12766754&dopt=Abstract
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Antihypertensive efficacy and safety of olmesartan medoxomil compared with amlodipine for mild-to-moderate hypertension. Author(s): Chrysant SG, Marbury TC, Robinson TD. Source: Journal of Human Hypertension. 2003 June; 17(6): 425-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764406&dopt=Abstract
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Are current strategies for treating hypertension effective? Author(s): Sica DA. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 May-June; 5(3 Suppl 2): 23-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826767&dopt=Abstract
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Are left ventricular mass, geometry and function related to vascular changes and/or insulin resistance in long-standing hypertension? ICARUS: a LIFE substudy. Author(s): Olsen MH, Hjerkinn E, Wachtell K, Hoieggen A, Bella JN, Nesbitt SD, Fossum E, Kjeldsen SE, Julius S, Ibsen H. Source: Journal of Human Hypertension. 2003 May; 17(5): 305-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756402&dopt=Abstract
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Are there differences in risk factor profiles and frequency of CT/MRI-based infarcts among African American stroke patients with and without hypertension? A report from the African American Antiplatelet Stroke Prevention Study (AAASPS). Author(s): Whittley CY, Gorelick PB, Raman R, Harris J, Richardson D. Source: Journal of the National Medical Association. 2003 June; 95(6): 423-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856908&dopt=Abstract
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Arm position and blood pressure: a risk factor for hypertension? Author(s): Mourad A, Carney S, Gillies A, Jones B, Nanra R, Trevillian P. Source: Journal of Human Hypertension. 2003 June; 17(6): 389-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764401&dopt=Abstract
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Assessing CHD and hypertension in minority ethnic communities. Author(s): Memon M, Abbas F, Memon B. Source: Nurs Times. 2003 April 22-28; 99(16): 26-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12739278&dopt=Abstract
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Assessment of the novel selective aldosterone blocker eplerenone using ambulatory and clinical blood pressure in patients with systemic hypertension. Author(s): White WB, Carr AA, Krause S, Jordan R, Roniker B, Oigman W. Source: The American Journal of Cardiology. 2003 July 1; 92(1): 38-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12842242&dopt=Abstract
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Association between hyperhomocysteinemia and primary pulmonary hypertension. Author(s): Arroliga AC, Sandur S, Jacobsen DW, Tewari S, Mustafa M, Mascha EJ, Robinson K. Source: Respiratory Medicine. 2003 July; 97(7): 825-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854633&dopt=Abstract
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Association between supine hypertension and orthostatic hypotension in autonomic failure. Author(s): Goldstein DS, Pechnik S, Holmes C, Eldadah B, Sharabi Y. Source: Hypertension. 2003 August; 42(2): 136-42. Epub 2003 June 30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835329&dopt=Abstract
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Associations of aortic and mitral regurgitation with body composition and myocardial energy expenditure in adults with hypertension: the Hypertension Genetic Epidemiology Network study. Author(s): Palmieri V, Bella JN, Arnett DK, Oberman A, Kitzman DW, Hopkins PN, Rao DC, Roman MJ, Devereux RB; Hypertension Genetic Epidemiology Network study. Source: American Heart Journal. 2003 June; 145(6): 1071-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796765&dopt=Abstract
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Atrial fibrillation: hypertension as a causative agent, risk factor for complications, and potential therapeutic target. Author(s): Healey JS, Connolly SJ. Source: The American Journal of Cardiology. 2003 May 22; 91(10A): 9G-14G. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781903&dopt=Abstract
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Atrial septostomy in the treatment of severe pulmonary arterial hypertension. Author(s): Reichenberger F, Pepke-Zaba J, McNeil K, Parameshwar J, Shapiro LM. Source: Thorax. 2003 September; 58(9): 797-800. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12947142&dopt=Abstract
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Back to the salt mines-- endothelial dysfunction in hypertension and compensatory role of endothelium-derived hyperpolarizing factor (EDHF). Author(s): Katusic ZS. Source: The Journal of Physiology. 2002 August 15; 543(Pt 1): 1. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12181276&dopt=Abstract
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Balance and gait in older adults with systemic hypertension. Author(s): Hausdorff JM, Herman T, Baltadjieva R, Gurevich T, Giladi N. Source: The American Journal of Cardiology. 2003 March 1; 91(5): 643-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12615286&dopt=Abstract
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Baroreflex sensitivity in essential and secondary hypertension. Author(s): Mussalo H, Vanninen E, Ikaheimo R, Laitinen T, Laakso M, Lansimies E, Hartikainen J. Source: Clinical Autonomic Research : Official Journal of the Clinical Autonomic Research Society. 2002 December; 12(6): 465-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12598951&dopt=Abstract
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Bartter's/Gitelman's syndrome: a model for the relationships between hypertension, angiotensin II, oxidative stress and remodeling. Author(s): Calo LA, Davis PA, Semplicini A. Source: Clinical Nephrology. 2003 May; 59(5): 393-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12779105&dopt=Abstract
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Benign intracranial hypertension and thyreostimulin suppression hormonotherapy. Author(s): Serratrice J, Granel B, Conrath J, Dufour H, Disdier P, Henry JF, Weiller PJ. Source: American Journal of Ophthalmology. 2002 December; 134(6): 910-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12470764&dopt=Abstract
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Benign intracranial hypertension in a patient with chronic renal failure, precipitated by hemodialysis. Author(s): Shaw D, Priestman W, McIntyre CW. Source: Clinical Nephrology. 2002 December; 58(6): 458-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508970&dopt=Abstract
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Benign intracranial hypertension in association with acute lymphoblastic leukemia. Author(s): Sastry J, Karandikar SS, English MW. Source: Pediatric Hematology and Oncology. 2003 March; 20(2): 157-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12554527&dopt=Abstract
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Beraprost sodium for pulmonary hypertension with congenital heart disease. Author(s): Suzuki H, Sato S, Tanabe S, Hayasaka K. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 2002 October; 44(5): 528-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12225555&dopt=Abstract
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Beraprost therapy for pulmonary arterial hypertension. Author(s): Barst RJ, McGoon M, McLaughlin V, Tapson V, Rich S, Rubin L, Wasserman K, Oudiz R, Shapiro S, Robbins IM, Channick R, Badesch D, Rayburn BK, Flinchbaugh R, Sigman J, Arneson C, Jeffs R; Beraprost Study Group. Source: Journal of the American College of Cardiology. 2003 June 18; 41(12): 2119-25. Erratum In: J Am Coll Cardiol. 2003 August 6; 42(3): 591. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12821234&dopt=Abstract
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Beyond hypertension: unraveling the causes of intracerebral hemorrhage. Author(s): Rosand J, Greenberg SM. Source: Stroke; a Journal of Cerebral Circulation. 2002 May; 33(5): 1195-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12532961&dopt=Abstract
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Bilateral adrenal masses in a patient with pregnancy-induced hypertension. Author(s): Eng S, Elias AN. Source: International Journal of Gynaecology and Obstetrics: the Official Organ of the International Federation of Gynaecology and Obstetrics. 2002 December; 79(3): 253-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12445994&dopt=Abstract
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Bilateral cannulation of internal jugular veins may worsen intracranial hypertension. Author(s): Stocchetti N, Longhi L, Valeriani V. Source: Anesthesiology. 2003 October; 99(4): 1017-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14508338&dopt=Abstract
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Bilateral cystic adenomatoid lung malformation type III--a rare differential diagnosis of pulmonary hypertension in neonates. Author(s): Banerjea MC, Wirbelauer J, Adam P, Trusen A, Marx A, Speer C. Source: Journal of Perinatal Medicine. 2002; 30(5): 429-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12442610&dopt=Abstract
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Bilateral renal embolization in the treatment of patients with renal insufficiency and arterial hypertension: report of a case of polycystic kidneys. Author(s): Basile A, Boullosa-Seoane E, Dominiguez-Viguera L, Certo A, Casal-Rivas M. Source: Radiol Med (Torino). 2002 May-June; 103(5-6): 555-7. English, Italian. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12207195&dopt=Abstract
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Bimatoprost 0.03% versus travoprost 0.004% in black Americans with glaucoma or ocular hypertension. Author(s): Noecker RJ, Earl ML, Mundorf T, Peace J, Williams RD. Source: Adv Ther. 2003 March-April; 20(2): 121-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12836812&dopt=Abstract
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Binswanger's disease: its association with hypertension and obstructive sleep apnea. Author(s): Matthews KD, Richter RW. Source: J Okla State Med Assoc. 2003 June; 96(6): 265-8; Quiz 269-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12858817&dopt=Abstract
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Biochemical endothelial markers and cardiovascular remodeling in refractory arterial hypertension. Author(s): Cittadino M, Goncalves de Sousa M, Ugar-Toledo JC, Rocha JC, Tanus-Santos JE, Moreno H Jr. Source: Clinical and Experimental Hypertension (New York, N.Y. : 1993). 2003 January; 25(1): 25-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12597522&dopt=Abstract
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Biofeedback of baroreflex sensitivity in patients with mild essential hypertension. Author(s): Overhaus S, Ruddel H, Curio I, Mussgay L, Scholz OB. Source: International Journal of Behavioral Medicine. 2003; 10(1): 66-78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581949&dopt=Abstract
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Biological factors are more important than socio-demographic and psychosocial conditions in relation to hypertension in middle-aged women. The Women's Health in the Lund Area (WHILA) study. Author(s): Lidfeldt J, Nyberg P, Nerbrand C, Ojehagen A, Samsioe G, Schersten B, Agardh CD. Source: Blood Pressure. 2002; 11(5): 270-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12458649&dopt=Abstract
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Birthweight, childhood growth and hypertension in adulthood. Author(s): Zhao M, Shu XO, Jin F, Yang G, Li HL, Liu DK, Wen W, Gao YT, Zheng W. Source: International Journal of Epidemiology. 2002 October; 31(5): 1043-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12435782&dopt=Abstract
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Blockade of the renin-angiotensin system in African Americans with hypertension and cardiovascular disease. Author(s): Saunders E, Gavin JR 3rd. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 January-February; 5(1 Suppl 1): 12-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12556668&dopt=Abstract
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Blockade of the renin-angiotensin system increases adiponectin concentrations in patients with essential hypertension. Author(s): Furuhashi M, Ura N, Higashiura K, Murakami H, Tanaka M, Moniwa N, Yoshida D, Shimamoto K. Source: Hypertension. 2003 July; 42(1): 76-81. Epub 2003 June 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796280&dopt=Abstract
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Blood lead levels and hypertension. Author(s): Hense HW. Source: Jama : the Journal of the American Medical Association. 2003 July 23; 290(4): 460; Author Reply 461. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12876084&dopt=Abstract
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Blood lead levels and hypertension. Author(s): Heaney RP. Source: Jama : the Journal of the American Medical Association. 2003 July 23; 290(4): 460-1; Author Reply 461. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12876083&dopt=Abstract
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Blood lead, blood pressure, and hypertension in perimenopausal and postmenopausal women. Author(s): Nash D, Magder L, Lustberg M, Sherwin RW, Rubin RJ, Kaufmann RB, Silbergeld EK. Source: Jama : the Journal of the American Medical Association. 2003 March 26; 289(12): 1523-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672769&dopt=Abstract
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Blood pressure and decline in kidney function: findings from the Systolic Hypertension in the Elderly Program (SHEP). Author(s): Young JH, Klag MJ, Muntner P, Whyte JL, Pahor M, Coresh J. Source: Journal of the American Society of Nephrology : Jasn. 2002 November; 13(11): 2776-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12397049&dopt=Abstract
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Blood pressure control and rates of edema following the administration of the cyclooxygenase-2 specific inhibitors celecoxib versus rofecoxib in patients with systemic hypertension and osteoarthritis. Author(s): Weaver A, Alderman M, Sperling R. Source: The American Journal of Cardiology. 2003 May 15; 91(10): 1291-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745131&dopt=Abstract
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Blood pressure increase and incidence of hypertension in relation to inflammationsensitive plasma proteins. Author(s): Engstrom G, Janzon L, Berglund G, Lind P, Stavenow L, Hedblad B, Lindgarde F. Source: Arteriosclerosis, Thrombosis, and Vascular Biology. 2002 December 1; 22(12): 2054-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12482834&dopt=Abstract
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Blood pressure reactivity to mental stress task as a determinant of sustained hypertension after 5 years of follow-up. Author(s): Armario P, del Rey RH, Martin-Baranera M, Almendros MC, Ceresuela LM, Pardell H. Source: Journal of Human Hypertension. 2003 March; 17(3): 181-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12624608&dopt=Abstract
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Blood pressure response after two-step exercise as a powerful predictor of hypertension: the Osaka Health Survey. Author(s): Tsumura K, Hayashi T, Hamada C, Endo G, Fujii S, Okada K. Source: Journal of Hypertension. 2002 August; 20(8): 1507-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12172311&dopt=Abstract
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Blood pressure-lowering effects of biofeedback treatment in hypertension: a metaanalysis of randomized controlled trials. Author(s): Nakao M, Yano E, Nomura S, Kuboki T. Source: Hypertens Res. 2003 January; 26(1): 37-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12661911&dopt=Abstract
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Blunted coronary vasoreactivity to insulin is an early alteration in hypertension. Author(s): Sundell J, Laine H, Luotolahti M, Nuutila P, Kalliokoski K, Raitakari O, Knuuti J. Source: Journal of Vascular Research. 2003 January-February; 40(1): 58-67. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12644726&dopt=Abstract
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BMPR2 germline mutations in pulmonary hypertension associated with fenfluramine derivatives. Author(s): Humbert M, Deng Z, Simonneau G, Barst RJ, Sitbon O, Wolf M, Cuervo N, Moore KJ, Hodge SE, Knowles JA, Morse JH. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2002 September; 20(3): 518-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12358323&dopt=Abstract
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Body mass index is the main risk factor for arterial hypertension in young subjects without major comorbidity. Author(s): Lukas A, Kumbein F, Temml C, Mayer B, Oberbauer R. Source: European Journal of Clinical Investigation. 2003 March; 33(3): 223-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12641540&dopt=Abstract
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Bone disorders, hypertension, and mitochondrial toxicity in HIV disease. Author(s): Newman MD. Source: Topics in Hiv Medicine : a Publication of the International Aids Society, Usa. 2003 January-February; 11(1): 10-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12717045&dopt=Abstract
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Bosentan for the treatment of pulmonary arterial hypertension. Author(s): Kenyon KW, Nappi JM. Source: The Annals of Pharmacotherapy. 2003 July-August; 37(7-8): 1055-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841819&dopt=Abstract
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Brainstem mechanisms of hypertension: role of the rostral ventrolateral medulla. Author(s): Sved AF, Ito S, Sved JC. Source: Current Hypertension Reports. 2003 June; 5(3): 262-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724060&dopt=Abstract
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Brimonidine Purite and bimatoprost compared with timolol and latanoprost in patients with glaucoma and ocular hypertension. Author(s): Netland PA, Michael M, Rosner SA, Katzman B, Macy JI. Source: Adv Ther. 2003 January-February; 20(1): 20-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12772815&dopt=Abstract
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Bronchopulmonary shunts in patients with chronic thromboembolic pulmonary hypertension: evaluation with helical CT and MR imaging. Author(s): Ley S, Kreitner KF, Morgenstern I, Thelen M, Kauczor HU. Source: Ajr. American Journal of Roentgenology. 2002 November; 179(5): 1209-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12388501&dopt=Abstract
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By the way, doctor. When I was first diagnosed with hypertension, my doctor (who knew that I was a competitive cyclist) prescribed an ACE inhibitor. I wondered for some time why he didn't prescribe diuretics, since all the articles I've read recommend that as a beginning step. Then I read in a bicycling magazine that ACE inhibitors are the only hypertension medicine that doesn't interfere with aerobic performance. Is that true? And did my doctor do the right thing? Author(s): Lee TH. Source: Harvard Health Letter / from Harvard Medical School. 2003 June; 28(8): 8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835145&dopt=Abstract
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Calcium antagonists in the treatment of hypertension in patients with ischaemic heart disease. Author(s): Rosendorff C. Source: Expert Opinion on Pharmacotherapy. 2003 September; 4(9): 1535-41. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12943483&dopt=Abstract
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Calcium channel blockers as the treatment of choice for hypertension in renal transplant recipients: fact or fiction. Author(s): Baroletti SA, Gabardi S, Magee CC, Milford EL. Source: Pharmacotherapy. 2003 June; 23(6): 788-801. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820820&dopt=Abstract
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Cardiac and vascular pathophysiology in hypertension. Author(s): Mayet J, Hughes A. Source: Heart (British Cardiac Society). 2003 September; 89(9): 1104-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12923045&dopt=Abstract
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Cardiovascular disease, hypertension, and lipids. Author(s): Watkins PJ. Source: Bmj (Clinical Research Ed.). 2003 April 19; 326(7394): 874-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12702626&dopt=Abstract
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Cardiovascular risk factors in children with obesity, hypertension and diabetes: lipoprotein(a) levels and body mass index correlate with family history of cardiovascular disease. Author(s): Glowinska B, Urban M, Koput A. Source: European Journal of Pediatrics. 2002 October; 161(10): 511-8. Epub 2002 August 30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12297895&dopt=Abstract
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Case 4: eruption on the face of a diabetic man suffering from retinopathy, hypertension, and nephropathy. Diagnosis: ciclosporin-associated hyperplastic folliculitis. Author(s): Harman KE, Higgins EM. Source: Clinical and Experimental Dermatology. 2003 May; 28(3): 341-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12780737&dopt=Abstract
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Central nervous system effects of moxonidine experimental sustained release formulation in patients with mild to moderate essential hypertension. Author(s): Kemme MJ, vd Post JP, Schoemaker RC, Straub M, Cohen AF, van Gerven JM. Source: British Journal of Clinical Pharmacology. 2003 June; 55(6): 518-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12814444&dopt=Abstract
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Change in cardiovascular risk profile by echocardiography in low- or medium-risk hypertension. Author(s): Schillaci G, De Simone G, Reboldi G, Porcellati C, Devereux RB, Verdecchia P. Source: Journal of Hypertension. 2002 August; 20(8): 1519-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12172313&dopt=Abstract
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Chocolate and blood pressure in elderly individuals with isolated systolic hypertension. Author(s): Taubert D, Berkels R, Roesen R, Klaus W. Source: Jama : the Journal of the American Medical Association. 2003 August 27; 290(8): 1029-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12941673&dopt=Abstract
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Classification of visual field abnormalities in the ocular hypertension treatment study. Author(s): Keltner JL, Johnson CA, Cello KE, Edwards MA, Bandermann SE, Kass MA, Gordon MO; Ocular Hypertension Treatment Study Group. Source: Archives of Ophthalmology. 2003 May; 121(5): 643-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742841&dopt=Abstract
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Clinical and therapeutical follow-up of HIV-associated pulmonary hypertension: prospective study of 10 patients. Author(s): Recusani F, Di Matteo A, Gambarin F, D'Armini A, Klersy C, Campana C. Source: Aids (London, England). 2003 April; 17 Suppl 1: S88-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12870536&dopt=Abstract
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Clinical significance of normalization of uterine artery pulsatility index with maternal heart rate for the evaluation of uterine circulation in pregnancy-induced hypertension. Author(s): Ochi H, Kusanagi Y, Katayama T, Matsubara K, Ito M. Source: Ultrasound in Obstetrics & Gynecology : the Official Journal of the International Society of Ultrasound in Obstetrics and Gynecology. 2003 May; 21(5): 459-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12768557&dopt=Abstract
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Clinical trials in isolated systolic hypertension in the elderly. Author(s): Garcia-Palmieri MR, Torrado JM. Source: P R Health Sci J. 2003 June; 22(2): 145-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12866138&dopt=Abstract
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Clinical trials: Evidence and unanswered questions--hypertension. Author(s): Celermajer DS. Source: Cerebrovascular Diseases (Basel, Switzerland). 2003; 16 Suppl 3: 18-24. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740552&dopt=Abstract
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Colonic wall thickening in patients with cirrhosis and portal hypertension. Author(s): Quilez C, Palazon JM, Arenas J, Alonso S, Sanchez J, Belda G, Perez-Mateo M. Source: Rev Esp Enferm Dig. 2003 April; 95(4): 269-72, 265-8. English, Spanish. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828526&dopt=Abstract
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Combination ACE inhibitors and angiotensin II receptor blockers for hypertension. Author(s): Finnegan PM, Gleason BL. Source: The Annals of Pharmacotherapy. 2003 June; 37(6): 886-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12773079&dopt=Abstract
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Combination therapy for hypertension: an update. Author(s): Moser M. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 July-August; 5(4): 247-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939563&dopt=Abstract
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Commentary on "Embracing complexity: A consideration of hypertension in the very old". Author(s): Lowenthal DT. Source: The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2003 July; 58(7): 664-5; Discussion 669-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865488&dopt=Abstract
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Commentary on "Embracing complexity: A consideration of hypertension in the very old". Author(s): Hajjar RR. Source: The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2003 July; 58(7): 661-2; Discussion 669-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865486&dopt=Abstract
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Commentary on "Embracing complexity: A consideration of hypertension in the very old". Author(s): Aronow WS. Source: The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2003 July; 58(7): 659-60; Discussion 669-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865484&dopt=Abstract
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Commentary on "Embracing complexity: A consideration of hypertension in the very old". Author(s): Newman AB. Source: The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2003 July; 58(7): 666-7; Discussion 669-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865490&dopt=Abstract
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Commentary on "Embracing complexity: A consideration of hypertension in the very old". Author(s): Michel JP, Grab B, Perrenoud JJ. Source: The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2003 July; 58(7): 665-6; Discussion 669-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865489&dopt=Abstract
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Comparative effect of lercanidipine, felodipine, and nifedipine GITS on blood pressure and heart rate in patients with mild to moderate arterial hypertension: the Lercanidipine in Adults (LEAD) Study. Author(s): Romito R, Pansini MI, Perticone F, Antonelli G, Pitzalis M, Rizzon P. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 July-August; 5(4): 249-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939564&dopt=Abstract
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Comparison of ambulatory blood pressure values in patients with glaucoma and ocular hypertension. Author(s): Yazici B, Usta E, Erturk H, Dilek K. Source: Eye (London, England). 2003 July; 17(5): 593-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12855965&dopt=Abstract
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Comparison of candesartan with lisinopril on ambulatory blood pressure and morning surge in patients with systemic hypertension. Author(s): Eguchi K, Kario K, Shimada K. Source: The American Journal of Cardiology. 2003 September 1; 92(5): 621-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12943892&dopt=Abstract
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Comparison of effects on systolic and diastolic left ventricular function of nebivolol versus atenolol in patients with uncomplicated essential hypertension. Author(s): Kamp O, Sieswerda GT, Visser CA. Source: The American Journal of Cardiology. 2003 August 1; 92(3): 344-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12888152&dopt=Abstract
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Comparison of patients with acute coronary syndrome with and without systemic hypertension. Author(s): Majahalme SK, Smith DE, Cooper JV, Kline-Rogers E, Mehta RH, Eagle KA, Bisognano JD. Source: The American Journal of Cardiology. 2003 August 1; 92(3): 258-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12888127&dopt=Abstract
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Comparison of the blood pressure-lowering effects and tolerability of Losartan- and Amlodipine-based regimens in patients with isolated systolic hypertension. Author(s): Volpe M, Junren Z, Maxwell T, Rodriguez A, Gamboa R, Gomez-Fernandez P, Ortega-Gonzalez G, Matadamas N, Rodriguez F, Dass B, Kyle C, Clarysse L, Bryce A, Moreno-Heredia E, Germano G, Gilles L, Smith RD, Sanderson JE; CDSP-944 Study Group. Source: Clinical Therapeutics. 2003 May; 25(5): 1469-89. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12867222&dopt=Abstract
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Compensatory mechanisms in patients with benign intracranial hypertension syndrome. Author(s): Gasparian SS, Serova NK, Sherbakova EY, Belova TN. Source: Acta Neurochir Suppl. 2002; 81: 31-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12171062&dopt=Abstract
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Complete remission of hypertension after successful living donation of a kidney with a large benign cyst. Author(s): Veroux P, Veroux M. Source: Transplantation. 2002 September 15; 74(5): 744. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12352897&dopt=Abstract
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Completely skewed X-inactivation in a mentally retarded young female with pseudohypoparathyroidism type IB and juvenile renin-dependent hypertension. Author(s): Demura M, Takeda Y, Yoneda T, Furukawa K, Tachi A, Mabuchi H. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 July; 88(7): 3043-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12843141&dopt=Abstract
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Compliance--and improving it--in hypertension. Author(s): Elliott WJ. Source: Manag Care. 2003 August; 12(8 Suppl Hypertension): 56-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12971594&dopt=Abstract
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Complications of hypertension as encountered by primary care physician. Author(s): Biswas S, Dastidar DG, Roy KS, Pal SK, Biswas TK, Ganguly SB. Source: J Indian Med Assoc. 2003 April; 101(4): 257-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12964646&dopt=Abstract
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Concurrent transcatheter closure of an apical muscular ventricular septal defect and a patent ductus arteriosus in a child with severe hyperkinetic pulmonary hypertension. Author(s): Joseph G, Muthunayagam JV, Mandalay A. Source: Pediatric Cardiology. 2003 January-February; 24(1): 47-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574978&dopt=Abstract
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Continuity of care and recognition of diabetes, hypertension, and hypercholesterolemia. Author(s): Koopman RJ, Mainous AG 3rd, Baker R, Gill JM, Gilbert GE. Source: Archives of Internal Medicine. 2003 June 9; 163(11): 1357-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796073&dopt=Abstract
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Contribution of salt intake to insulin resistance associated with hypertension. Author(s): Ogihara T, Asano T, Fujita T. Source: Life Sciences. 2003 June 20; 73(5): 509-23. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12770608&dopt=Abstract
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Coronary vasodilator capacity and hypertension-induced increase in left ventricular mass. Author(s): Kozakova M, de Simone G, Morizzo C, Palombo C. Source: Hypertension. 2003 February; 41(2): 224-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574086&dopt=Abstract
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COX-2-specific inhibitors and the kidney: effect on hypertension and oedema. Author(s): Whelton A. Source: Journal of Hypertension. 2002 September; 20 Suppl 6: S31-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12683425&dopt=Abstract
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Current perspectives on arterial stiffness and pulse pressure in hypertension and cardiovascular diseases. Author(s): Safar ME, Levy BI, Struijker-Boudier H. Source: Circulation. 2003 June 10; 107(22): 2864-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796414&dopt=Abstract
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Current treatment of patients with hypertension: therapeutic implications of INSIGHT. Author(s): Taddei S, Ghiadoni L, Salvetti A. Source: Drugs. 2003; 63(14): 1435-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12834362&dopt=Abstract
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Data access. Industry groups petition for data on salt and hypertension. Author(s): Kaiser J. Source: Science. 2003 May 30; 300(5624): 1350. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775802&dopt=Abstract
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Decompressive laparotomy: a novel approach in the management of severe intracranial hypertension. Author(s): Miglietta MA, Salzano LJ, Chiu WC, Scalea TM. Source: The Journal of Trauma. 2003 September; 55(3): 551-4; Discussion 554-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14501902&dopt=Abstract
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Design and statistical aspects of the African American Study of Kidney Disease and Hypertension (AASK). Author(s): Gassman JJ, Greene T, Wright JT Jr, Agodoa L, Bakris G, Beck GJ, Douglas J, Jamerson K, Lewis J, Kutner M, Randall OS, Wang SR. Source: Journal of the American Society of Nephrology : Jasn. 2003 July; 14(7 Suppl 2): S154-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12819322&dopt=Abstract
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Detectable serum cardiac troponin T as a marker of poor prognosis among patients with chronic precapillary pulmonary hypertension. Author(s): Torbicki A, Kurzyna M, Kuca P, Fijalkowska A, Sikora J, Florczyk M, Pruszczyk P, Burakowski J, Wawrzynska L. Source: Circulation. 2003 August 19; 108(7): 844-8. Epub 2003 Aug 04. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12900346&dopt=Abstract
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Detection of incipient left ventricular hypertrophy in mild to moderate arterial hypertension with normal electrocardiogram and echocardiogram: a new use for signal-averaged electrocardiography. Author(s): Ginefra P, Barbosa EC, Barbosa PR, Bomfim AS, Boghossian SH, Salgado AA, Brasil FG, Freitas EA, Albanesi Filho FM. Source: Arquivos Brasileiros De Cardiologia. 2003 July; 81(1): 79-84, 73-8. Epub 2003 July 31. English, Portuguese. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12908075&dopt=Abstract
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Determinants of elevated pulse pressure in middle-aged and older subjects with uncomplicated systolic hypertension: the role of proximal aortic diameter and the aortic pressure-flow relationship. Author(s): Mitchell GF, Lacourciere Y, Ouellet JP, Izzo JL Jr, Neutel J, Kerwin LJ, Block AJ, Pfeffer MA. Source: Circulation. 2003 September 30; 108(13): 1592-8. Epub 2003 Sep 15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12975261&dopt=Abstract
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Determinants of poor hypertension management in the community. Author(s): Maziak W, Keil U, Doring A, Hense HW. Source: Journal of Human Hypertension. 2003 March; 17(3): 215-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12624614&dopt=Abstract
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Development of congestive heart failure in type 2 diabetic patients with microalbuminuria or proteinuria: observations from the DIABHYCAR (type 2 DIABetes, Hypertension, CArdiovascular Events and Ramipril) study. Author(s): Vaur L, Gueret P, Lievre M, Chabaud S, Passa P; DIABHYCAR Study Group (type 2 DIABetes, Hypertension, CARdiovascular Events and Ramipril) study. Source: Diabetes Care. 2003 March; 26(3): 855-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610049&dopt=Abstract
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Devices and techniques for blood pressure measurement and criteria for hypertension adopted by Brazilian physicians: exploratory study. Author(s): Mion D Jr, Pierin AM, Lessa I, Nobre F. Source: Arquivos Brasileiros De Cardiologia. 2002 December; 79(6): 597-600, 593-6. English, Portuguese. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12532243&dopt=Abstract
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Dexamethasone induction of hypertension and diabetes is PPAR-alpha dependent in LDL receptor-null mice. Author(s): Bernal-Mizrachi C, Weng S, Feng C, Finck BN, Knutsen RH, Leone TC, Coleman T, Mecham RP, Kelly DP, Semenkovich CF. Source: Nature Medicine. 2003 August; 9(8): 1069-75. Epub 2003 July 06. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847522&dopt=Abstract
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Diabetes and hypertension in severe obesity and effects of gastric bypass-induced weight loss. Author(s): Sugerman HJ, Wolfe LG, Sica DA, Clore JN. Source: Annals of Surgery. 2003 June; 237(6): 751-6; Discussion 757-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796570&dopt=Abstract
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Diabetes, hypertension and birth injuries: a complex interrelationship. Author(s): Iffy L, Djordjevic MM, Apuzzio JJ, Martin JD, Sama JC. Source: Med Law. 2003; 22(2): 207-19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12889640&dopt=Abstract
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Diagnosing secondary hypertension. Author(s): Onusko E. Source: American Family Physician. 2003 January 1; 67(1): 67-74. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12537168&dopt=Abstract
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Diagnosis and evaluation of pulmonary hypertension. Author(s): Budev MM, Arroliga AC, Jennings CA. Source: Cleve Clin J Med. 2003 April; 70 Suppl 1: S9-17. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716138&dopt=Abstract
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Diagnosis and management of gestational hypertension and preeclampsia. Author(s): Sibai BM. Source: Obstetrics and Gynecology. 2003 July; 102(1): 181-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12850627&dopt=Abstract
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Diagnosis and treatment of hypertension in children and adolescents. Author(s): Peters RM, Flack JM. Source: Journal of the American Academy of Nurse Practitioners. 2003 February; 15(2): 56-63. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640940&dopt=Abstract
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Diagnosis of portopulmonary hypertension in candidates for liver transplantation: a prospective study. Author(s): Colle IO, Moreau R, Godinho E, Belghiti J, Ettori F, Cohen-Solal A, Mal H, Bernuau J, Marty J, Lebrec D, Valla D, Durand F. Source: Hepatology (Baltimore, Md.). 2003 February; 37(2): 401-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12540791&dopt=Abstract
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Dietary markers of hypertension associated with pulse pressure and arterial compliance in black South African children: the THUSA Bana Study. Author(s): Schutte AE, Van Rooyen JM, Huisman HW, Kruger HS, Malan NT, De Ridder JH. Source: Cardiovasc J S Afr. 2003 March-April; 14(2): 81-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12748745&dopt=Abstract
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Dietary protein and hypertension: where do we stand? Author(s): Martin DS. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2003 April; 19(4): 385-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12679176&dopt=Abstract
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Dietary risk markers that contribute to the aetiology of hypertension in black South African children: the THUSA BANA study. Author(s): Schutte AE, van Rooyen JM, Huisman HW, Kruger HS, Malan NT, De Ridder JH; Transition and Health During Urbanisation in South Africa in Children; Bana: Children. Source: Journal of Human Hypertension. 2003 January; 17(1): 29-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571614&dopt=Abstract
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Dietary salt and hypertension: a scientific issue or a matter of faith? Author(s): Robertson JI. Source: Journal of Evaluation in Clinical Practice. 2003 February; 9(1): 1-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12558698&dopt=Abstract
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Differential influence of family history of hypertension and premature myocardial infarction on systolic blood pressure and left ventricular mass trajectories in youth. Author(s): Dekkers JC, Treiber FA, Kapuku G, Snieder H. Source: Pediatrics. 2003 June; 111(6 Pt 1): 1387-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12777557&dopt=Abstract
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Digestive endoscopy and portal hypertension. North Italian Endoscopic Club. Author(s): Cestari R, Minelli L, Lanzini A, Missale G, Ravelli P, Salerni B. Source: Ital J Gastroenterol. 1996 November; 28 Suppl 2: 18-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14509962&dopt=Abstract
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Diminished renal kallikrein responses to mineralocorticoid stimulation in African Americans: determinants of an intermediate phenotype for hypertension. Author(s): Wong CM, O'Connor DT, Martinez JA, Kailasam MT, Parmer RJ. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2003 April; 16(4): 281-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12670744&dopt=Abstract
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Dispersion method of excessive portal hypertension (shear stress) and changes of portal pressure and flow after living-related liver transplantation with a splenorenal shunt: a case report. Author(s): Hara Y, Sato Y, Yamamoto S, Nakatsuka H, Takeishi T, Hirano K, Kobayashi T, Watanabe T, Hatakeyama K. Source: Transplantation Proceedings. 2003 February; 35(1): 414-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12591466&dopt=Abstract
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Do community based self-reading sphygmomanometers improve detection of hypertension? A feasibility study. Author(s): Hamilton W, Round A, Goodchild R, Baker C. Source: Journal of Public Health Medicine. 2003 June; 25(2): 125-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12848401&dopt=Abstract
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Do hypertension and diuretic treatment in pregnancy increase the risk of schizophrenia in offspring? Author(s): Sorensen HJ, Mortensen EL, Reinisch JM, Mednick SA. Source: The American Journal of Psychiatry. 2003 March; 160(3): 464-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12611826&dopt=Abstract
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Does a prolonged QT peak identify left ventricular hypertrophy in hypertension? Author(s): Wong KY, Lim PO, Wong SY, MacWalter RS, Struthers AD, MacDonald TM. Source: International Journal of Cardiology. 2003 June; 89(2-3): 179-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767541&dopt=Abstract
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Does orthostatic hypotension predict the occurrence of nocturnal arterial hypertension in the elderly patient? Author(s): Carmona J, Amado P, Vasconcelos N, Almeida L, Santos I, Alves J, Nazare J. Source: Rev Port Cardiol. 2003 May; 22(5): 607-15. English, Portuguese. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12940176&dopt=Abstract
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Doppler tissue imaging reveals systolic dysfunction in patients with hypertension and apparent "isolated" diastolic dysfunction. Author(s): Poulsen SH, Andersen NH, Ivarsen PI, Mogensen CE, Egeblad H. Source: Journal of the American Society of Echocardiography : Official Publication of the American Society of Echocardiography. 2003 July; 16(7): 724-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835658&dopt=Abstract
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Doxycycline induced intracranial hypertension. Author(s): Lochhead J, Elston JS. Source: Bmj (Clinical Research Ed.). 2003 March 22; 326(7390): 641-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649241&dopt=Abstract
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Drug treatment of hypertension. Conclusion of editorial is somewhat flawed. Author(s): Hackam DG. Source: Bmj (Clinical Research Ed.). 2003 April 5; 326(7392): 764. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12676853&dopt=Abstract
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Drug treatment of hypertension: implications of ALLHAT. Author(s): Williams B. Source: Heart (British Cardiac Society). 2003 June; 89(6): 589-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12748205&dopt=Abstract
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Drug treatment of mild hypertension in elderly--we should be cautious in some patients. Author(s): Singh AK, Singh M. Source: J Assoc Physicians India. 2002 October; 50: 1340; Author Reply 1340-1. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12568237&dopt=Abstract
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Drug-induced hypertension. Author(s): Handler J. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 January-February; 5(1): 83-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12556663&dopt=Abstract
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Drugs that interrupt the renin-angiotensin system should be among the preferred initial drugs to treat hypertension. Author(s): Moore MA. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 March-April; 5(2): 137-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671327&dopt=Abstract
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Early posttransplantation hypertension and poor long-term renal allograft survival in pediatric patients. Author(s): Mitsnefes MM, Khoury PR, McEnery PT. Source: The Journal of Pediatrics. 2003 July; 143(1): 98-103. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915832&dopt=Abstract
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Eclampsia in Southern Alberta: is there a role for seizure prophylaxis in all women with gestational hypertension? Author(s): Foong SC, Pollard JK. Source: J Obstet Gynaecol Can. 2003 May; 25(5): 385-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738979&dopt=Abstract
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Economics of suboptimal drug use: cost-savings of using JNC-recommended medications for management of uncomplicated essential hypertension. Author(s): Xu KT, Moloney M, Phillips S. Source: Am J Manag Care. 2003 August; 9(8): 529-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12921230&dopt=Abstract
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Effect of a hypertension teaching protocol on patient and staff satisfaction in a rural community health center. Author(s): Stanton MP, Nix GS. Source: Lippincott's Case Management : Managing the Process of Patient Care. 2003 May-June; 8(3): 125-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12777973&dopt=Abstract
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Effect of beta-blockers on peripheral skin microcirculation in hypertension and peripheral vascular disease. Author(s): Ubbink DT, Verhaar EE, Lie HK, Legemate DA. Source: Journal of Vascular Surgery : Official Publication, the Society for Vascular Surgery [and] International Society for Cardiovascular Surgery, North American Chapter. 2003 September; 38(3): 535-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12947273&dopt=Abstract
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Effect of nitroglycerin inhalation on patients with pulmonary hypertension undergoing mitral valve replacement surgery. Author(s): Yurtseven N, Karaca P, Kaplan M, Ozkul V, Tuygun AK, Aksoy T, Canik S, Kopman E. Source: Anesthesiology. 2003 October; 99(4): 855-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14508317&dopt=Abstract
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Effect of orally active prostacyclin analogue on survival in patients with chronic thromboembolic pulmonary hypertension without major vessel obstruction. Author(s): Ono F, Nagaya N, Okumura H, Shimizu Y, Kyotani S, Nakanishi N, Miyatake K. Source: Chest. 2003 May; 123(5): 1583-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740277&dopt=Abstract
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Effects of enalapril on left ventricular mass and diastolic function in essential hypertension: special reference to duration of hypertension. Author(s): Oki T, Fukuda N, Iuchi A, Tabata T, Sasaki M, Kawahara K, Ishimoto T, Tominaga T, Okushi H, Fujimoto T, Ito S. Source: Journal of Cardiac Failure. 1995 December; 1(5): 365-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12836711&dopt=Abstract
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Effects of exercise and weight loss on hypertension. Author(s): Beilin LJ, Burke V, Puddey IB. Source: Jama : the Journal of the American Medical Association. 2003 August 20; 290(7): 887; Author Reply 887-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928461&dopt=Abstract
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Effects of exercise and weight loss on hypertension. Author(s): Yeo S. Source: Jama : the Journal of the American Medical Association. 2003 August 20; 290(7): 886; Author Reply 886-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928460&dopt=Abstract
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Effects of exercise and weight loss on hypertension. Author(s): McCarthy WJ, Arpawong TE, Dietsch BJ, Yancey AK. Source: Jama : the Journal of the American Medical Association. 2003 August 20; 290(7): 885; Author Reply 886-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928458&dopt=Abstract
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Effects of exercise and weight loss on hypertension. Author(s): Blumenthal JA, Sherwood A, Bacon SL, Hinderliter A. Source: Jama : the Journal of the American Medical Association. 2003 August 20; 290(7): 885-6; Author Reply 886-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928457&dopt=Abstract
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Effects of hemorheological factors on the development of hypertension in diabetic children. Author(s): Cam H, Pusuroglu K, Aydin A, Ercan M. Source: Journal of Tropical Pediatrics. 2003 June; 49(3): 164-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12848207&dopt=Abstract
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Effects of hypertension and obesity on endometrial thickness. Author(s): Serdar Serin I, Ozcelik B, Basbug M, Ozsahin O, Yilmazsoy A, Erez R. Source: European Journal of Obstetrics, Gynecology, and Reproductive Biology. 2003 July 1; 109(1): 72-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12818448&dopt=Abstract
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Effects of telmisartan and losartan on left ventricular mass in mild-to-moderate hypertension. A randomized, double-blind trial. Author(s): Martina B, Dieterle T, Sigle JP, Surber C, Battegay E. Source: Cardiology. 2003; 99(3): 169-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12824726&dopt=Abstract
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Effects of the Dietary Approaches to Stop Hypertension (DASH) diet on the pressurenatriuresis relationship. Author(s): Akita S, Sacks FM, Svetkey LP, Conlin PR, Kimura G; DASH-Sodium Trial Collaborative Research Group. Source: Hypertension. 2003 July; 42(1): 8-13. Epub 2003 May 19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756219&dopt=Abstract
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Effects of the dual endothelin receptor antagonist bosentan in patients with pulmonary arterial hypertension: a 1-year follow-up study. Author(s): Sitbon O, Badesch DB, Channick RN, Frost A, Robbins IM, Simonneau G, Tapson VF, Rubin LJ. Source: Chest. 2003 July; 124(1): 247-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12853530&dopt=Abstract
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Efficacy and tolerability of fixed-dose combinations of telmisartan plus HCTZ compared with losartan plus HCTZ in patients with essential hypertension. Author(s): Lacourciere Y, Gil-Extremera B, Mueller O, Byrne M, Williams L. Source: Int J Clin Pract. 2003 May; 57(4): 273-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12800457&dopt=Abstract
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Efficacy of moderate hypothermia in patients with severe head injury and intracranial hypertension refractory to mild hypothermia. Author(s): Shiozaki T, Nakajima Y, Taneda M, Tasaki O, Inoue Y, Ikegawa H, Matsushima A, Tanaka H, Shimazu T, Sugimoto H. Source: Journal of Neurosurgery. 2003 July; 99(1): 47-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854743&dopt=Abstract
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Efficacy of nephrectomy for the treatment of nephrogenic hypertension in a pediatric population. Author(s): Baez-Trinidad LG, Lendvay TS, Broecker BH, Smith EA, Warshaw BL, Hymes L, Kirsch AJ. Source: The Journal of Urology. 2003 October; 170(4 Pt 2): 1655-7; Discussion 1658. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14501684&dopt=Abstract
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Elevated plasma fibrinogen levels in patients with essential hypertension are related to vascular complications. Author(s): Lechi C, Gaino S, Zuliani V, Tommasoli RM, Faccini G, Fasson R, Arcaro G, Lechi A, Minuz P. Source: International Angiology : a Journal of the International Union of Angiology. 2003 March; 22(1): 72-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771860&dopt=Abstract
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Elevated serum concentrations of androgens in women with pregnancy-induced hypertension. Author(s): Jirecek S, Joura EA, Tempfer C, Knofler M, Husslein P, Zeisler H. Source: Wiener Klinische Wochenschrift. 2003 March 31; 115(5-6): 162-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12741075&dopt=Abstract
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Embracing complexity: A consideration of hypertension in the very old. Author(s): Goodwin JS. Source: The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2003 July; 58(7): 653-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865483&dopt=Abstract
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Emerging therapies for pulmonary hypertension: striving for efficacy and safety. Author(s): Kao PN, Faul JL. Source: Journal of the American College of Cardiology. 2003 June 18; 41(12): 2126-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12821235&dopt=Abstract
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Endoscopic ligation of esophageal varices for prophylaxis of first bleeding in children and adolescents with portal hypertension: preliminary results of a prospective study. Author(s): Celinska-Cedro D, Teisseyre M, Woynarowski M, Socha P, Socha J, Ryzko J. Source: Journal of Pediatric Surgery. 2003 July; 38(7): 1008-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861528&dopt=Abstract
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Evaluation of patient counseling on blood pressure control of out-patients with hypertension at Chulalongkorn Hospital. Author(s): Aramwit P, Assawawitoontip S. Source: J Med Assoc Thai. 2003 June; 86 Suppl 2: S496-500. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12930031&dopt=Abstract
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Evaluation of renal causes of hypertension. Author(s): Hartman RP, Kawashima A, King BF Jr. Source: Radiologic Clinics of North America. 2003 September; 41(5): 909-29. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14521201&dopt=Abstract
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Evidence-based treatment of hypertension. JNC 7 Guidelines provide an updated framework. Author(s): Lookinland S, Beckstrand RL. Source: Adv Nurse Pract. 2003 September; 11(9): 32-9; Quiz 39-40. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14521107&dopt=Abstract
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Exercise training counteracts the abnormal release of plasma endothelin-1 in normal subjects at risk for hypertension. Author(s): Tanzilli G, Barilla F, Pannitteri G, Greco C, Comito C, Schiariti M, Papalia U, Mangieri E. Source: Ital Heart J. 2003 February; 4(2): 107-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12762273&dopt=Abstract
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Expression of human herpesvirus 8 in primary pulmonary hypertension. Author(s): Cool CD, Rai PR, Yeager ME, Hernandez-Saavedra D, Serls AE, Bull TM, Geraci MW, Brown KK, Routes JM, Tuder RM, Voelkel NF. Source: The New England Journal of Medicine. 2003 September 18; 349(12): 1113-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13679525&dopt=Abstract
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Factor analysis of possible risks for hypertension in a black South African population. Author(s): Schutte AE, van Rooyen JM, Huisman HW, Kruger HS, de Ridder JH. Source: Journal of Human Hypertension. 2003 May; 17(5): 339-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756407&dopt=Abstract
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Factors associated with uncontrolled hypertension in an affluent, elderly population. Author(s): Inciardi JF, McMahon K, Sauer BL. Source: The Annals of Pharmacotherapy. 2003 April; 37(4): 485-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12659600&dopt=Abstract
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Factors influencing arterial stiffness in systolic hypertension in the elderly: role of sodium and the renin-angiotensin system. Author(s): Safar ME, Benetos A. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2003 March; 16(3): 249-58. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12620707&dopt=Abstract
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Fall in mean arterial pressure and fetal growth restriction in pregnancy hypertension: an updated metaregression analysis. Author(s): von Dadelszen P, Magee LA. Source: J Obstet Gynaecol Can. 2002 December; 24(12): 941-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12464992&dopt=Abstract
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Familial aggregation of diabetes and hypertension in a case-control study of colorectal neoplasia. Author(s): Brauer PM, McKeown-Eyssen GE, Jazmaji V, Logan AG, Andrews DF, Jenkins D, Marcon N, Saibil F, Cohen L, Stern H, Baron D, Greenberg G, Diamandis E, Kakis G, Singer W, Steiner G. Source: American Journal of Epidemiology. 2002 October 15; 156(8): 702-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12370158&dopt=Abstract
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Familial hyperkalemic hypertension: phenotypic analysis in a large family with the WNK1 deletion mutation. Author(s): Achard JM, Warnock DG, Disse-Nicodeme S, Fiquet-Kempf B, Corvol P, Fournier A, Jeunemaitre X. Source: The American Journal of Medicine. 2003 April 15; 114(6): 495-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727582&dopt=Abstract
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Familial idiopathic intracranial hypertension. Author(s): Karaman K, Gverovic-Antunica A, Zuljan I, Vukojevic N, Zoltner B, Erceg I, Ivkosic A. Source: Croatian Medical Journal. 2003 August; 44(4): 480-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950154&dopt=Abstract
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Familial/sporadic glucocorticoid resistance syndrome and hypertension. Author(s): Kino T, Vottero A, Charmandari E, Chrousos GP. Source: Annals of the New York Academy of Sciences. 2002 September; 970: 101-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12381545&dopt=Abstract
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Family history of hypertension and type 2 diabetes in relation to preeclampsia risk. Author(s): Qiu C, Williams MA, Leisenring WM, Sorensen TK, Frederick IO, Dempsey JC, Luthy DA. Source: Hypertension. 2003 March; 41(3): 408-13. Epub 2003 February 17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623936&dopt=Abstract
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Fibromuscular dysplasia in renovascular hypertension demonstrated by multislice CT: comparison with conventional angiogram and intravascular ultrasound. Author(s): Funabashi N, Komiyama N, Komuro I. Source: Heart (British Cardiac Society). 2003 June; 89(6): 639. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12748219&dopt=Abstract
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Fish consumption and hypertension incidence in African Americans and whites: the NHANES I Epidemiologic Follow-up Study. Author(s): Gillum RF, Mussolino ME, Madans JH. Source: Journal of the National Medical Association. 2001 April; 93(4): 124-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653399&dopt=Abstract
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Fixed combination trandolapril/verapamil sustained-release: a review of its use in essential hypertension. Author(s): Muijsers RB, Curran MP, Perry CM. Source: Drugs. 2002; 62(17): 2539-67. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12421112&dopt=Abstract
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Fixed combinations of delapril plus indapamide vs fosinopril plus hydrochlorothiazide in mild to moderate essential hypertension. Author(s): Cremonesi G, Cavalieri L, Cikes I, Dobovisek J, Bacchelli S, Degli Esposti D, Costa FV, Borghi C, Ambrosioni E. Source: Adv Ther. 2002 May-June; 19(3): 129-37. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12201354&dopt=Abstract
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For the patient. Are vegetarians at less risk for obesity, diabetes, and hypertension? Obesity, diabetes, hypertension, and vegetarian status among Seventh-Day Adventists in Barbados: preliminary results. Author(s): Brathwaite N, Fraser HS, Modeste N, Broome H, King R. Source: Ethn Dis. 2003 Winter; 13(1): 148. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723025&dopt=Abstract
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For the patient. The effectiveness of a community health worker outreach program on healthcare utilization of west Baltimore City Medicaid patients with diabetes, with or without hypertension. Author(s): Fedder DO, Chang RJ, Curry S, Nichols G. Source: Ethn Dis. 2003 Winter; 13(1): 146. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723023&dopt=Abstract
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Forearm vasoconstriction to endothelin-1 is impaired, but constriction to sarafotoxin 6c and vasodilatation to BQ-123 unaltered, in patients with essential hypertension. Author(s): Ferro CJ, Haynes WG, Hand MF, Webb DJ. Source: Clinical Science (London, England : 1979). 2002 August; 103 Suppl 48: 53S-58S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12193054&dopt=Abstract
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Forms of mineralocorticoid hypertension. Author(s): Ferrari P, Bonny O. Source: Vitam Horm. 2003; 66: 113-56. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12852254&dopt=Abstract
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Frequency and severity of tricuspid regurgitation determined by Doppler echocardiography in primary pulmonary hypertension. Author(s): Hinderliter AL, Willis PW 4th, Long WA, Clarke WR, Ralph D, Caldwell EJ, Williams W, Ettinger NA, Hill NS, Summer WR, de Boisblanc B, Koch G, Li S, Clayton LM, Jobsis MM, Crow JW; PPH Study Group. Source: The American Journal of Cardiology. 2003 April 15; 91(8): 1033-7, A9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12686360&dopt=Abstract
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Frequency doubling perimetry in ocular hypertension and chronic open angle glaucoma. Author(s): Cellini M, Torreggiani A. Source: Acta Ophthalmologica Scandinavica. Supplement. 2002; 236: 24-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390120&dopt=Abstract
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Frequency doubling technology and high-pass resolution perimetry in glaucoma and ocular hypertension. Author(s): Kalaboukhova L, Lindblom B. Source: Acta Ophthalmologica Scandinavica. 2003 June; 81(3): 247-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12780403&dopt=Abstract
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Frequency of analgesic use and risk of hypertension in younger women. Author(s): Curhan GC, Willett WC, Rosner B, Stampfer MJ. Source: Archives of Internal Medicine. 2002 October 28; 162(19): 2204-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390063&dopt=Abstract
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From linkage to genes in human hypertension. Author(s): Melander O. Source: Journal of Hypertension. 2002 November; 20(11): 2135-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12409946&dopt=Abstract
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From theory into practice: arterial haemodynamics in clinical hypertension. Author(s): O'Rourke MF. Source: Journal of Hypertension. 2002 October; 20(10): 1901-15. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12359961&dopt=Abstract
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Function of the serotonin 5-hydroxytryptamine 2B receptor in pulmonary hypertension. Author(s): Launay JM, Herve P, Peoc'h K, Tournois C, Callebert J, Nebigil CG, Etienne N, Drouet L, Humbert M, Simonneau G, Maroteaux L. Source: Nature Medicine. 2002 October; 8(10): 1129-35. Epub 2002 September 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12244304&dopt=Abstract
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Functional heterogeneity of bone morphogenetic protein receptor-II mutants found in patients with primary pulmonary hypertension. Author(s): Nishihara A, Watabe T, Imamura T, Miyazono K. Source: Molecular Biology of the Cell. 2002 September; 13(9): 3055-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12221115&dopt=Abstract
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Gamma-glutamyltransferase is a predictor of incident diabetes and hypertension: the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Author(s): Lee DH, Jacobs DR Jr, Gross M, Kiefe CI, Roseman J, Lewis CE, Steffes M. Source: Clinical Chemistry. 2003 August; 49(8): 1358-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12881453&dopt=Abstract
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Gastrectomy in combination with a distal splenorenal shunt in a patient with gastric cancer and portal hypertension: report of a case. Author(s): Kato T, Kato H, Kondo S, Okushiba S, Morikawa T. Source: Surgery Today. 2002; 32(8): 727-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12181726&dopt=Abstract
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Gastric motility in patients with presinusoidal portal hypertension. Author(s): Aprile LR, Meneghelli UG, Martinelli AL, Monteiro CR. Source: The American Journal of Gastroenterology. 2002 December; 97(12): 3038-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492187&dopt=Abstract
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Gender and age differences in lifestyle factors related to hypertension in middle-aged civil service employees. Author(s): Hori Y, Toyoshima H, Kondo T, Tamakoshi K, Yatsuya H, Zhu S, Kawamura T, Toyama J, Okamoto N. Source: J Epidemiol. 2003 January; 13(1): 38-47. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12587612&dopt=Abstract
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Gender, age and deprivation differences in the primary care management of hypertension in Scotland: a cross-sectional database study. Author(s): Pears E, Hannaford PC, Taylor MW. Source: Family Practice. 2003 February; 20(1): 22-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509366&dopt=Abstract
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Gender-specific correlates of leptin with hypertension-related phenotypes in African Americans. Author(s): El-Gharbawy AH, Kotchen JM, Grim CE, Kaldunski M, Hoffmann RG, Pausova Z, Hamet P, Kotchen TA. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2002 November; 15(11): 989-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12441220&dopt=Abstract
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Gene expression profiling in hypertension research: a critical perspective. Author(s): Pravenec M, Wallace C, Aitman TJ, Kurtz TW. Source: Hypertension. 2003 January; 41(1): 3-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12511522&dopt=Abstract
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Gene polymorphisms of the renin-angiotensin-aldosterone system and essential arterial hypertension in childhood. Author(s): Petrovic D, Bidovec M, Peterlin B. Source: Folia Biol (Krakow). 2002; 50(1-2): 53-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12597535&dopt=Abstract
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Gene transfer of human guanosine 5'-triphosphate cyclohydrolase I restores vascular tetrahydrobiopterin level and endothelial function in low renin hypertension. Author(s): Zheng JS, Yang XQ, Lookingland KJ, Fink GD, Hesslinger C, Kapatos G, Kovesdi I, Chen AF. Source: Circulation. 2003 September 9; 108(10): 1238-45. Epub 2003 August 18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12925450&dopt=Abstract
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Gene-targeting studies of the renin-angiotensin system: mechanisms of hypertension and cardiovascular disease. Author(s): Gurley SB, Le TH, Coffman TM. Source: Cold Spring Harb Symp Quant Biol. 2002; 67: 451-7. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12858571&dopt=Abstract
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Genetic basis of essential hypertension in Tibetan. Author(s): Zhuang L, Cui C, Chen Y, Cen W, Qiu C, Xu Q, Liu Y, Zhu X, Fang M, Wu Z. Source: Zhonghua Yi Xue Za Zhi. 2002 August 10; 82(15): 1009-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12194787&dopt=Abstract
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Genetic influences in human hypertension. Author(s): Rutherford PA. Source: Journal of Hypertension. 2003 January; 21(1): 19-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12544427&dopt=Abstract
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Genetic studies of pulmonary arterial hypertension. Author(s): Morse JH. Source: Lupus. 2003; 12(3): 209-12. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12708784&dopt=Abstract
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Genetic variants of WNK4 in whites and African Americans with hypertension. Author(s): Erlich PM, Cui J, Chazaro I, Farrer LA, Baldwin CT, Gavras H, DeStefano AL. Source: Hypertension. 2003 June; 41(6): 1191-5. Epub 2003 April 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12719438&dopt=Abstract
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Genetics and pulmonary hypertension. Author(s): Loyd JE. Source: Chest. 2002 December; 122(6 Suppl): 284S-286S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12475800&dopt=Abstract
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Genetics of essential hypertension: from families to genes. Author(s): Barlassina C, Lanzani C, Manunta P, Bianchi G. Source: Journal of the American Society of Nephrology : Jasn. 2002 November; 13 Suppl 3: S155-64. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12466306&dopt=Abstract
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Genetics of hypertension: the adducin paradigm. Author(s): Bianchi G, Tripodi G. Source: Annals of the New York Academy of Sciences. 2003 April; 986: 660-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763916&dopt=Abstract
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Genetics of pulmonary hypertension: from bench to bedside. Author(s): Humbert M, Trembath RC. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2002 September; 20(3): 741-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12358355&dopt=Abstract
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Genetics of the kidney and hypertension. Author(s): Watson B Jr. Source: Current Hypertension Reports. 2003 June; 5(3): 273-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724062&dopt=Abstract
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Genome scans for hypertension and blood pressure regulation. Author(s): Samani NJ. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2003 February; 16(2): 167-71. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12559688&dopt=Abstract
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Genome-wide linkage analyses for hypertension genes in two ethnically and geographically diverse populations. Author(s): Kardia SL, Rozek LS, Krushkal J, Ferrell RE, Turner ST, Hutchinson R, Brown A, Sing CF, Boerwinkle E. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2003 February; 16(2): 154-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12559685&dopt=Abstract
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Genome-wide mapping of human loci for essential hypertension. Author(s): Caulfield M, Munroe P, Pembroke J, Samani N, Dominiczak A, Brown M, Benjamin N, Webster J, Ratcliffe P, O'Shea S, Papp J, Taylor E, Dobson R, Knight J, Newhouse S, Hooper J, Lee W, Brain N, Clayton D, Lathrop GM, Farrall M, Connell J; MRC British Genetics of Hypertension Study. Source: Lancet. 2003 June 21; 361(9375): 2118-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826435&dopt=Abstract
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Genomic medicine: exploring the basis of a new approach to endocrine hypertension. Author(s): Alesci S, Chrousos GP, Pacak K. Source: Annals of the New York Academy of Sciences. 2002 September; 970: 177-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12381553&dopt=Abstract
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Genotyping of essential hypertension single-nucleotide polymorphisms by a homogeneous PCR method with universal energy transfer primers. Author(s): Bengra C, Mifflin TE, Khripin Y, Manunta P, Williams SM, Jose PA, Felder RA. Source: Clinical Chemistry. 2002 December; 48(12): 2131-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446468&dopt=Abstract
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Goal-oriented hypertension management: translating clinical trials to practice. Author(s): Singer GM, Izhar M, Black HR. Source: Hypertension. 2002 October; 40(4): 464-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12364348&dopt=Abstract
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Goldblatt's kidney, Hughes syndrome and hypertension. Author(s): Sangle S, D'Cruz D, Khamashta M, Tungekar MF, Abbs I, Hughes G. Source: Lupus. 2002; 11(11): 699-703. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12474999&dopt=Abstract
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G-protein beta3 subunit 825T allele and hypertension. Author(s): Siffert W. Source: Current Hypertension Reports. 2003 February; 5(1): 47-53. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12530935&dopt=Abstract
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Graded balloon atrial septostomy in severe pulmonary hypertension. Author(s): Tandon R. Source: Indian Heart J. 2002 May-June; 54(3): 326; Author Reply 326. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12216938&dopt=Abstract
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Growth and living conditions in childhood and hypertension in adult life: a longitudinal study. Author(s): Barker DJ, Forsen T, Eriksson JG, Osmond C. Source: Journal of Hypertension. 2002 October; 20(10): 1951-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12359972&dopt=Abstract
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Guidelines for treatment of hypertension in the elderly--2002 revised version. Author(s): Ogihara T, Hiwada K, Morimoto S, Matsuoka H, Matsumoto M, Takishita S, Shimamoto K, Shimada K, Abe I, Ouchi Y, Tsukiyama H, Katayama S, Imai Y, Suzuki H, Kohara K, Okaishi K, Mikami H. Source: Hypertens Res. 2003 January; 26(1): 1-36. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12661910&dopt=Abstract
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Haemodynamic comparison of amlodipine and atenolol in essential hypertension using the quantascope. Author(s): Tham TC, Herity N, Guy S, Silke B. Source: British Journal of Clinical Pharmacology. 1993 December; 36(6): 555-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12959272&dopt=Abstract
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Headache as a predictive factor of severe systolic hypertension in acute ischemic stroke. Author(s): Hong YH, Lee YS, Park SH. Source: The Canadian Journal of Neurological Sciences. Le Journal Canadien Des Sciences Neurologiques. 2003 August; 30(3): 210-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12945943&dopt=Abstract
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Help! Grandma's stroking: Balancing morbidity and mortality in the treatment of hypertension among the very old. Author(s): Denson S. Source: The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2003 July; 58(7): 660-1; Discussion 669-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865485&dopt=Abstract
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Hemodynamic and catecholamine responses during tracheal intubation using a lightwand device (Trachlight) in elderly patients with hypertension. Author(s): Kanaide M, Fukusaki M, Tamura S, Takada M, Miyako M, Sumikawa K. Source: Journal of Anesthesia. 2003; 17(3): 161-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12911202&dopt=Abstract
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Hemolytic anemia-associated pulmonary hypertension of sickle cell disease and the nitric oxide/arginine pathway. Author(s): Jison ML, Gladwin MT. Source: American Journal of Respiratory and Critical Care Medicine. 2003 July 1; 168(1): 3-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826592&dopt=Abstract
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Homocysteine plasma concentration levels for the prediction of preeclampsia in women with chronic hypertension. Author(s): Zeeman GG, Alexander JM, McIntire DD, Devaraj S, Leveno KJ. Source: American Journal of Obstetrics and Gynecology. 2003 August; 189(2): 574-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14520237&dopt=Abstract
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How well are hypertension and albuminuria treated in type II diabetic patients? Author(s): Boero R, Prodi E, Elia F, Porta L, Martelli S, Ferraro L, Quarello F. Source: Journal of Human Hypertension. 2003 June; 17(6): 413-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764404&dopt=Abstract
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Hybrid cell-gene therapy for pulmonary hypertension based on phagocytosing action of endothelial progenitor cells. Author(s): Nagaya N, Kangawa K, Kanda M, Uematsu M, Horio T, Fukuyama N, Hino J, Harada-Shiba M, Okumura H, Tabata Y, Mochizuki N, Chiba Y, Nishioka K, Miyatake K, Asahara T, Hara H, Mori H. Source: Circulation. 2003 August 19; 108(7): 889-95. Epub 2003 June 30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835224&dopt=Abstract
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Hydralazine for treatment of severe hypertension in pregnancy: meta-analysis. Author(s): Magee LA, Cham C, Waterman EJ, Ohlsson A, von Dadelszen P. Source: Bmj (Clinical Research Ed.). 2003 October 25; 327(7421): 955-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14576246&dopt=Abstract
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Hyperhomocysteinemia but not MTHFR genotype is associated with young-onset essential hypertension. Author(s): Garfunkel VA, Porto PI, Garcia SI, Dieuzeide G, Kirszner T, Plotquin Y, Spataro RJ, Gonzalez C, Pirola CJ. Source: Journal of Human Hypertension. 2003 May; 17(5): 361-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756410&dopt=Abstract
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Hyperhomocysteinemia in menopausal hypertension: an added risk factor and a dangerous association for organ damage. Author(s): Noto R, Neri S, Molino G, Meli S, Noto P, Mauceri B, Cilio D, Rapisarda A, Noto Z. Source: Eur Rev Med Pharmacol Sci. 2002 July-August; 6(4): 81-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12729036&dopt=Abstract
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Hypertension and cancer mortality: is there a place for antioxidant interventions? Author(s): Korantzopoulos P, Papaioannides D. Source: Indian Heart J. 2003 January-February; 55(1): 95-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760600&dopt=Abstract
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Hypertension and cognitive function: pathophysiologic effects of hypertension on the brain. Author(s): Manolio TA, Olson J, Longstreth WT. Source: Current Hypertension Reports. 2003 June; 5(3): 255-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724059&dopt=Abstract
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Hypertension and diabetes mellitus. Author(s): Jayakumar RV. Source: J Indian Med Assoc. 2003 April; 101(4): 254-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12964645&dopt=Abstract
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Hypertension and heart failure sine heart failure. The ACC/AHA guidelines: a misadventure in the lexicography of cardiomyopathy and heart failure, particularly for the hypertensive. Author(s): Giles TD. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 July-August; 5(4): 280-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939569&dopt=Abstract
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Hypertension and obesity. Author(s): Najman DM, Kapoor P, Serrano A, Tckachenko D. Source: Archives of Internal Medicine. 2003 May 12; 163(9): 1114-5; Author Reply 1115-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742816&dopt=Abstract
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Hypertension and renal dysfunction: NHANES III. Author(s): Jones CA. Source: Journal of the American Society of Nephrology : Jasn. 2003 July; 14(7 Suppl 2): S71-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12819306&dopt=Abstract
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Hypertension and the cortisol-cortisone shuttle. Author(s): Quinkler M, Stewart PM. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 June; 88(6): 2384-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788832&dopt=Abstract
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Hypertension and the prothrombotic state. Author(s): Nadar S, Lip GY. Source: Journal of the American College of Cardiology. 2003 May 21; 41(10): 1847; Author Reply 1847. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767675&dopt=Abstract
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Hypertension in diabetes. Author(s): Sahay BK, Sahay RK. Source: J Indian Med Assoc. 2003 January; 101(1): 12, 14-5, 44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841500&dopt=Abstract
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Hypertension in older urban Native-American primary care patients. Author(s): Rhoades DA, Buchwald D. Source: Journal of the American Geriatrics Society. 2003 June; 51(6): 774-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12757563&dopt=Abstract
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Hypertension in the athlete. Author(s): Sachtleben T, Fields KB. Source: Curr Sports Med Rep. 2003 April; 2(2): 79-83. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12831663&dopt=Abstract
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Hypertension prevalence and blood pressure levels in 6 European countries, Canada, and the United States. Author(s): Wolf-Maier K, Cooper RS, Banegas JR, Giampaoli S, Hense HW, Joffres M, Kastarinen M, Poulter N, Primatesta P, Rodriguez-Artalejo F, Stegmayr B, Thamm M, Tuomilehto J, Vanuzzo D, Vescio F. Source: Jama : the Journal of the American Medical Association. 2003 May 14; 289(18): 2363-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746359&dopt=Abstract
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Hypertension prevalence and stroke mortality across populations. Author(s): Staessen JA, Kuznetsova T, Stolarz K. Source: Jama : the Journal of the American Medical Association. 2003 May 14; 289(18): 2420-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746368&dopt=Abstract
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Hypertension update: lessons from the literature. Author(s): Ong HT. Source: Med J Malaysia. 2002 December; 57(4): 510-4. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12733181&dopt=Abstract
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Hypertension, diabetes, and longitudinal changes in intraocular pressure. Author(s): Hennis A, Wu SY, Nemesure B, Leske MC; Barbados Eye Studies Group. Source: Ophthalmology. 2003 May; 110(5): 908-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750088&dopt=Abstract
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Hypertension, obesity, and the renin-angiotensin system: a tale of tight associations. Author(s): Sibley S. Source: Minn Med. 2003 January; 86(1): 46-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12585560&dopt=Abstract
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Hypertension: a review of therapeutic options. Author(s): Carter BL. Source: Manag Care. 2003 August; 12(8 Suppl Hypertension): 34-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12971591&dopt=Abstract
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Hypertension: prevalence and economic implications. Author(s): Dalzell MD. Source: Manag Care. 2003 August; 12(8 Suppl Hypertension): 6-11. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12971587&dopt=Abstract
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Hypertension: treating the patient as well as the blood pressure. Author(s): Jackson G. Source: Int J Clin Pract. 2003 June; 57(5): 357. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846335&dopt=Abstract
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Identifying at-risk patients through community pharmacy-based hypertension and stroke prevention screening projects. Author(s): Mangum SA, Kraenow KR, Narducci WA. Source: Journal of the American Pharmaceutical Association (Washington,D.C. : 1996). 2003 January-February; 43(1): 50-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12585751&dopt=Abstract
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Idiopathic intracranial hypertension in the pediatric population. Author(s): Ng YT, Bodensteiner JB. Source: Journal of Child Neurology. 2003 June; 18(6): 440; Author Reply 440. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12886985&dopt=Abstract
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Idiopathic intracranial hypertension: associations with coagulation disorders and polycystic-ovary syndrome. Author(s): Glueck CJ, Iyengar S, Goldenberg N, Smith LS, Wang P. Source: The Journal of Laboratory and Clinical Medicine. 2003 July; 142(1): 35-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12878984&dopt=Abstract
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Image of the month. Superior mesenteric arteriovenous fistula and portal hypertension. Author(s): Revilla Jde L, Herreros de Tejada A, Garrido A. Source: Gastroenterology. 2003 September; 125(3): 653, 1000. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949709&dopt=Abstract
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Immediate and long-term hemodynamic and clinical effects of sildenafil in patients with pulmonary arterial hypertension receiving vasodilator therapy. Author(s): Bhatia S, Frantz RP, Severson CJ, Durst LA, McGoon MD. Source: Mayo Clinic Proceedings. 2003 October; 78(10): 1207-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14531479&dopt=Abstract
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Immune cell CD62L and CD11a expression in response to a psychological stressor in human hypertension. Author(s): Mills PJ, Farag NH, Hong S, Kennedy BP, Berry CC, Ziegler MG. Source: Brain, Behavior, and Immunity. 2003 August; 17(4): 260-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12831828&dopt=Abstract
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Implementing a shared-care approach to improve the management of patients with pulmonary arterial hypertension. Author(s): Mughal MM, Mandell B, James K, Stelmach K, Minai OA. Source: Cleve Clin J Med. 2003 April; 70 Suppl 1: S28-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716140&dopt=Abstract
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Improvement of microcirculation and healing of venous hypertension and ulcers with Crystacide. Evaluation of free radicals, laser Doppler flux and PO2. A prospectiverandomized-controlled study. Author(s): Belcaro G, Cesarone MR, Nicolaides AN, Geroulakos G, Di Renzo A, Milani M, Ricci A, Brandolini R, Dugall M, Ruffini I, Cornelli U, Griffin M. Source: Angiology. 2003 May-June; 54(3): 325-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12785025&dopt=Abstract
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In vivo adaptive response of the peripheral conduit artery in patients with borderline systolic hypertension. Author(s): Tao J, Jin Y, Wang L, Tang A, Liao X, Yang Z, Ma H. Source: Chin Med J (Engl). 2003 March; 116(3): 333-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781031&dopt=Abstract
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Increased serum ferritin is common in men with essential hypertension. Author(s): Piperno A, Trombini P, Gelosa M, Mauri V, Pecci V, Vergani A, Salvioni A, Mariani R, Mancia G. Source: Journal of Hypertension. 2002 August; 20(8): 1513-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12172312&dopt=Abstract
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Infection-induced pulmonary hypertension crisis after Rastelli procedure. Author(s): Katoh Y, Nakajima Y, Yamagishi M, Mizobe T. Source: Paediatric Anaesthesia. 2003 June; 13(5): 461-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791125&dopt=Abstract
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Inferior meso-caval shunt for portal hypertension with bleeding esophageal varices. Author(s): Khanna R, Mishra S, Khanna S, Khanna AK. Source: Indian J Gastroenterol. 2003 May-June; 22(3): 108-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839390&dopt=Abstract
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Influence of antihypertensive medication on aldosterone and renin concentration in the differential diagnosis of essential hypertension and primary aldosteronism. Author(s): Seifarth C, Trenkel S, Schobel H, Hahn EG, Hensen J. Source: Clinical Endocrinology. 2002 October; 57(4): 457-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12354127&dopt=Abstract
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Inhibin-A and superimposed preeclampsia in women with chronic hypertension. Author(s): Zeeman GG, Alexander JM, McIntire DD, Byrd W, Leveno KJ. Source: Obstetrics and Gynecology. 2003 February; 101(2): 232-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12576244&dopt=Abstract
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Inhibition of 11beta-hydroxysteroid dehydrogenase type 1 lowers intraocular pressure in patients with ocular hypertension. Author(s): Rauz S, Cheung CM, Wood PJ, Coca-Prados M, Walker EA, Murray PI, Stewart PM. Source: Qjm : Monthly Journal of the Association of Physicians. 2003 July; 96(7): 481-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12881590&dopt=Abstract
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Initial management of ocular hypertension and primary open-angle glaucoma: an evaluation of the royal college of ophthalmologists' guidelines. Author(s): Choong YF, Devarajan N, Pickering A, Pickering S, Austin MW. Source: Eye (London, England). 2003 August; 17(6): 685-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928677&dopt=Abstract
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Initial treatment of hypertension. Author(s): Berend K. Source: The New England Journal of Medicine. 2003 September 11; 349(11): 1090-1; Author Reply 1090-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12971366&dopt=Abstract
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Initial treatment of hypertension. Author(s): Porat G. Source: The New England Journal of Medicine. 2003 September 11; 349(11): 1090-1; Author Reply 1090-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12968097&dopt=Abstract
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Initial treatment of hypertension. Author(s): August P. Source: The New England Journal of Medicine. 2003 February 13; 348(7): 610-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12584370&dopt=Abstract
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Insulin resistance and its potential role in pregnancy-induced hypertension. Author(s): Seely EW, Solomon CG. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 June; 88(6): 2393-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788833&dopt=Abstract
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Insulin resistance, hypertension, and coronary heart disease. Author(s): Reaven G. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 July-August; 5(4): 269-74. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939567&dopt=Abstract
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Insulin resistance/compensatory hyperinsulinemia, essential hypertension, and cardiovascular disease. Author(s): Reaven GM. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 June; 88(6): 2399403. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788834&dopt=Abstract
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Interactions between the renin-angiotensin system and dyslipidemia: relevance in the therapy of hypertension and coronary heart disease. Author(s): Singh BM, Mehta JL. Source: Archives of Internal Medicine. 2003 June 9; 163(11): 1296-304. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796065&dopt=Abstract
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Intraoperative management of severe pulmonary hypertension during cardiac surgery with inhaled iloprost. Author(s): Rex S, Busch T, Vettelschoss M, de Rossi L, Rossaint R, Buhre W. Source: Anesthesiology. 2003 September; 99(3): 745-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12960562&dopt=Abstract
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Is the 'rule of halves' in hypertension still valid?--Evidence from the Chennai Urban Population Study. Author(s): Deepa R, Shanthirani CS, Pradeepa R, Mohan V. Source: J Assoc Physicians India. 2003 February; 51: 153-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12725257&dopt=Abstract
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Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? Author(s): Johnson RJ, Kang DH, Feig D, Kivlighn S, Kanellis J, Watanabe S, Tuttle KR, Rodriguez-Iturbe B, Herrera-Acosta J, Mazzali M. Source: Hypertension. 2003 June; 41(6): 1183-90. Epub 2003 April 21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707287&dopt=Abstract
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Isolated systolic hypertension: analysis of a significant sample of the Portuguese population. Author(s): Ramalhinho V. Source: Rev Port Cardiol. 2003 January; 22(1): 25-6. English, Portuguese. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12712808&dopt=Abstract
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Isolated systolic hypertension: data on a cohort of young subjects from a French working population (IHPAF). Author(s): Mallion JM, Hamici L, Chatellier G, Lang T, Plouin PF, De Gaudemaris R. Source: Journal of Human Hypertension. 2003 February; 17(2): 93-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574786&dopt=Abstract
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Isolated systolic hypertension--epidemiology and impact in clinical practice. Author(s): Rocha E, Mello e Silva A, Gouveia-Oliveira A, Nogueira P. Source: Rev Port Cardiol. 2003 January; 22(1): 7-23. English, Portuguese. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12712807&dopt=Abstract
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Isovolume hypertonic solutes (sodium chloride or mannitol) in the treatment of refractory posttraumatic intracranial hypertension: 2 mL/kg 7.5% saline is more effective than 2 mL/kg 20% mannitol. Author(s): Vialet R, Albanese J, Thomachot L, Antonini F, Bourgouin A, Alliez B, Martin C. Source: Critical Care Medicine. 2003 June; 31(6): 1683-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794404&dopt=Abstract
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JNC 7 express: new thinking in hypertension treatment. Author(s): Green L. Source: American Family Physician. 2003 July 15; 68(2): 228, 230. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892344&dopt=Abstract
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JNC 7 urges aggressive management of hypertension. Author(s): Thompson CA. Source: American Journal of Health-System Pharmacy : Ajhp : Official Journal of the American Society of Health-System Pharmacists. 2003 June 15; 60(12): 1206, 1209. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12845912&dopt=Abstract
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J-shaped relationship in hypertension. Author(s): Simon G. Source: Annals of Internal Medicine. 2003 January 7; 138(1): 78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12513059&dopt=Abstract
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Key issues in the diagnosis and management of hypertension. Author(s): Yonga GO. Source: East Afr Med J. 2000 April; 77(4): 177-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12858898&dopt=Abstract
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Lack of association between angiotensin converting enzyme (ACE) genotype, serum ACE activity, and haemodynamics in patients with primary pulmonary hypertension. Author(s): Hoeper MM, Tacacs A, Stellmacher U, Lichtinghagen R. Source: Heart (British Cardiac Society). 2003 April; 89(4): 445-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12639879&dopt=Abstract
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Lack of association between angiotensin II type 1 receptor gene polymorphism and hypertension in Japanese. Author(s): Ono K, Mannami T, Baba S, Yasui N, Ogihara T, Iwai N. Source: Hypertens Res. 2003 February; 26(2): 131-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12627871&dopt=Abstract
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Lack of association between progressive supranuclear palsy and arterial hypertension: a clinicopathological study. Author(s): Colosimo C, Osaki Y, Vanacore N, Lees AJ. Source: Movement Disorders : Official Journal of the Movement Disorder Society. 2003 June; 18(6): 694-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12784275&dopt=Abstract
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Laparoscopic nephrectomy for renovascular hypertension in a 6-month-old infant. Author(s): Thomas PB, Hebra A, Chavin K. Source: Jsls. 2003 January-March; 7(1): 63-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723001&dopt=Abstract
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L-arginine transport in humans with cortisol-induced hypertension. Author(s): Chin-Dusting JP, Ahlers BA, Kaye DM, Kelly JJ, Whitworth JA. Source: Hypertension. 2003 June; 41(6): 1336-40. Epub 2003 April 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707296&dopt=Abstract
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Left atrial mechanical function in patients with essential hypertension. Author(s): Erol MK, Yilmaz M, Acikel M, Karakelleoglu S. Source: Acta Cardiol. 2002 October; 57(5): 323-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12405568&dopt=Abstract
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Left ventricle is better suited as pulmonary ventricle in simple transposition with severe pulmonary hypertension. Author(s): Sharma R, Choudhary SK, Bhan A, Juneja R, Kothari SS, Saxena A, Venugopal P. Source: The Annals of Thoracic Surgery. 2002 November; 74(5): 1612-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12440617&dopt=Abstract
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Left ventricular concentric geometry as a risk factor in gestational hypertension. Author(s): Novelli GP, Valensise H, Vasapollo B, Larciprete G, Altomare F, Di Pierro G, Casalino B, Galante A, Arduini D. Source: Hypertension. 2003 March; 41(3): 469-75. Epub 2003 February 17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623945&dopt=Abstract
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Left ventricular hypertrophy is associated with reduced vasodilatory capacity in the brachial artery in patients with longstanding hypertension. A LIFE substudy. Author(s): Olsen MH, Wachtell K, Hermann KL, Bella JN, Dige-Petersen H, Rokkedal J, Ibsen H. Source: Blood Pressure. 2002; 11(5): 285-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12458651&dopt=Abstract
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Left ventricular mass change during treatment and outcome in patients with essential hypertension. Author(s): Koren MJ, Ulin RJ, Koren AT, Laragh JH, Devereux RB. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2002 December; 15(12): 1021-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12460696&dopt=Abstract
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Left ventricular remodeling and renal function in never-treated essential hypertension. Author(s): Fesler P, Du Cailar G, Ribstein J, Mimran A. Source: Journal of the American Society of Nephrology : Jasn. 2003 April; 14(4): 881-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660322&dopt=Abstract
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Leptin and the central neural mechanisms of obesity hypertension. Author(s): Rahmouni K, G Haynes W. Source: Drugs Today (Barc). 2002 December; 38(12): 807-17. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582470&dopt=Abstract
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Lifestyle modifications to prevent hypertension. Author(s): Logan AG. Source: Jama : the Journal of the American Medical Association. 2003 February 19; 289(7): 843; Author Reply 843-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588260&dopt=Abstract
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Lifestyle modifications to prevent hypertension. Author(s): McGuffin M. Source: Jama : the Journal of the American Medical Association. 2003 February 19; 289(7): 843; Author Reply 843-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588259&dopt=Abstract
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Linkage analysis of five candidate genes and essential hypertension in 106 Chinese nuclear families. Author(s): He X, Wang G, Huang W, Ding-Liang Z. Source: Journal of Human Hypertension. 2003 January; 17(1): 69-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571619&dopt=Abstract
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Lipid lowering in hypertension and heart protection: observations from the AngloScandinavian Cardiac Outcomes Trial (ASCOT) and the Heart Protection Study. Author(s): Nadar S, Lim HS, Beevers DG, Lip GY. Source: Journal of Human Hypertension. 2002 December; 16(12): 815-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12522461&dopt=Abstract
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Lipid peroxidation is not increased in patients with untreated mild-to-moderate hypertension. Author(s): Cracowski JL, Baguet JP, Ormezzano O, Bessard J, Stanke-Labesque F, Bessard G, Mallion JM. Source: Hypertension. 2003 February; 41(2): 286-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574096&dopt=Abstract
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Living transplantation using a kidney with a large cyst as curative treatment of donor's hypertension. Author(s): Veroux P, Veroux M, Puliatti C, Macarone M, Sorbello M, Valvo MC, Cappello D. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2002 December; 17(12): 2258-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454244&dopt=Abstract
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Local cardiac renin-angiotensin system: hypertension and cardiac failure. Author(s): Varagic J, Frohlich ED. Source: Journal of Molecular and Cellular Cardiology. 2002 November; 34(11): 1435-42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12431442&dopt=Abstract
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Long-lasting improvement of arterial hypertension after surgical treatment of a foramen magnum meningioma: case report. Author(s): Worner BA, Rahim T, Lange M, Fink U, Oeckler R. Source: Surgical Neurology. 2002 September-October; 58(3-4): 189-92; Discussion 193. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12480212&dopt=Abstract
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Long-term treatment with oral sildenafil in addition to continuous IV epoprostenol in patients with pulmonary arterial hypertension. Author(s): Stiebellehner L, Petkov V, Vonbank K, Funk G, Schenk P, Ziesche R, Block LH. Source: Chest. 2003 April; 123(4): 1293-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684325&dopt=Abstract
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Long-time survival with HIV-related pulmonary arterial hypertension: a case report. Author(s): Alp S, Schlottmann R, Bauer TT, Schmidt WE, Bastian A. Source: Aids (London, England). 2003 July 25; 17(11): 1714-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12853763&dopt=Abstract
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Loosening the cuff: important new advances in modeling antihypertensive treatment effects in genetic studies of hypertension. Author(s): Palmer LJ. Source: Hypertension. 2003 February; 41(2): 197-8. Erratum In: Hypertension. 2003 March; 41(3): E3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574080&dopt=Abstract
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Low birth weight as a risk factor for hypertension. Author(s): Lackland DT, Egan BM, Ferguson PL. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 March-April; 5(2): 133-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671326&dopt=Abstract
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Low dose acetylsalicylic acid in prevention of pregnancy-induced hypertension and intrauterine growth retardation in women with bilateral uterine artery notches. Author(s): Smith JH. Source: Bjog : an International Journal of Obstetrics and Gynaecology. 2002 December; 109(12): 1421-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12510691&dopt=Abstract
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Low dose acetylsalicylic acid in prevention of pregnancy-induced hypertension and intrauterine growth retardation in women with bilateral uterine artery notches. Author(s): Coomarasamy A, Gee H, Khan KS. Source: Bjog : an International Journal of Obstetrics and Gynaecology. 2002 December; 109(12): 1420-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12504994&dopt=Abstract
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Low dose acetylsalicylic acid in prevention of pregnancy-induced hypertension and intrauterine growth retardation in women with bilateral uterine artery notches. Author(s): Somerset D. Source: Bjog : an International Journal of Obstetrics and Gynaecology. 2002 December; 109(12): 1420. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12504993&dopt=Abstract
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Low-density lipoprotein subfractions and cardiovascular risk in hypertension: relationship to endothelial dysfunction and effects of treatment. Author(s): Felmeden DC, Spencer CG, Blann AD, Beevers DG, Lip GY. Source: Hypertension. 2003 March; 41(3): 528-33. Epub 2003 February 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623954&dopt=Abstract
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Lower cognitive function in the presence of obesity and hypertension: the Framingham heart study. Author(s): Elias MF, Elias PK, Sullivan LM, Wolf PA, D'Agostino RB. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 February; 27(2): 260-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12587008&dopt=Abstract
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Lymphocyte subpopulations in pregnancy complicated by hypertension. Author(s): Mahmoud F, Omu A, Abul H, El-Rayes S, Haines D. Source: Journal of Obstetrics and Gynaecology : the Journal of the Institute of Obstetrics and Gynaecology. 2003 January; 23(1): 20-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623476&dopt=Abstract
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Malignant hypertension and hypertensive encephalopathy in primary aldosteronism caused by adrenal adenoma. Author(s): Bortolotto LA, Cesena FH, Jatene FB, Silva HB. Source: Arquivos Brasileiros De Cardiologia. 2003 July; 81(1): 97-100, 93-6. Epub 2003 July 31. English, Portuguese. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12908077&dopt=Abstract
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Malignant hypertension as a presenting symptom of Takayasu arteritis. Author(s): Wolak T, Szendro G, Golcman L, Paran E. Source: Mayo Clinic Proceedings. 2003 February; 78(2): 231-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12583535&dopt=Abstract
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Management of high blood pressure in African Americans: consensus statement of the Hypertension in African Americans Working Group of the International Society on Hypertension in Blacks. Author(s): Douglas JG, Bakris GL, Epstein M, Ferdinand KC, Ferrario C, Flack JM, Jamerson KA, Jones WE, Haywood J, Maxey R, Ofili EO, Saunders E, Schiffrin EL, Sica DA, Sowers JR, Vidt DG; Hypertension in African Americans Working Group of the International Society on Hypertension in Blacks. Source: Archives of Internal Medicine. 2003 March 10; 163(5): 525-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12622600&dopt=Abstract
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Management of hypertension and screening of renal complications by GPs in diabetic type 2 patients (France--2001). Author(s): Fagnani F, Souchet T, Labed D, Gaugris S, Hannedouche T, Grimaldi A. Source: Diabetes & Metabolism. 2003 February; 29(1): 58-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629449&dopt=Abstract
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Management of hypertension in light of the new national guidelines. Author(s): Moser M. Source: Manag Care. 2003 August; 12(8 Suppl Hypertension): 12-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12971588&dopt=Abstract
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Management of pulmonary hypertension: physiological and pharmacological considerations for anesthesiologists. Author(s): Fischer LG, Van Aken H, Burkle H. Source: Anesthesia and Analgesia. 2003 June; 96(6): 1603-16. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760982&dopt=Abstract
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Management of refractory hypertension. Author(s): Ram CV. Source: American Journal of Therapeutics. 2003 March-April; 10(2): 122-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629590&dopt=Abstract
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Managing hypertension in patients with stroke. Are you prepared for labetalol infusion? Author(s): Harrington C. Source: Critical Care Nurse. 2003 June; 23(3): 30-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830778&dopt=Abstract
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Managing hypertension. Author(s): Stanton AV. Source: The Practitioner. 2003 September; 247(1650): 712-5, 717-8, 721-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13677709&dopt=Abstract
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Managing hypertension: measurement and prevention. Author(s): Hurst R. Source: Nurs Times. 2002 September 17-23; 98(38): 38-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12355920&dopt=Abstract
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Managing hypertension--a real challenge in the new millennium. Author(s): Biswas TK, Biswas S. Source: J Indian Med Assoc. 2003 April; 101(4): 250. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12964643&dopt=Abstract
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Massive spontaneous perirenal hematoma and accelerated hypertension in a patient with polyarteritis nodosa. Author(s): Minardi D, Dessi-Fulgheri P, Sarzani R, Onesta M, Mucaj A, Branchi A, Giangiacomi M, Mantovani P, Muzzonigro G. Source: Urologia Internationalis. 2003; 70(3): 227-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660463&dopt=Abstract
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Measuring hypertension control: NCQA and beyond. Author(s): Miller NH. Source: Manag Care. 2003 August; 12(8 Suppl Hypertension): 51-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12971593&dopt=Abstract
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Measuring the habitat as an indicator of socioeconomic position: methodology and its association with hypertension. Author(s): Galobardes B, Morabia A. Source: Journal of Epidemiology and Community Health. 2003 April; 57(4): 248-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12646538&dopt=Abstract
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Membrane fluidity and hypertension. Author(s): Tsuda K, Nishio I. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2003 March; 16(3): 259-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12620708&dopt=Abstract
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Mendelian hypertension with brachydactyly as a molecular genetic lesson in regulatory physiology. Author(s): Luft FC, Toka O, Toka HR, Jordan J, Bahring S. Source: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 2003 October; 285(4): R709-14. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12959913&dopt=Abstract
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Mesalazine-associated benign intracranial hypertension in a patient with ulcerative colitis. Author(s): Rosa N, Giamundo A, Jura A, Iaccarino G, Romano A. Source: American Journal of Ophthalmology. 2003 July; 136(1): 212-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12834704&dopt=Abstract
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Mesenteric venous thrombosis causing jejunal stricture: secondary to hypercoagulable states and primary portal hypertension. Author(s): Chandra S, Dutta U, Das R, Vaiphei K, Nagi B, Singh K. Source: Digestive Diseases and Sciences. 2002 September; 47(9): 2017-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12353848&dopt=Abstract
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Metabolic abnormalities (hypertension, hyperglycemia and overweight), lifestyle (high energy intake and physical inactivity) and endometrial cancer risk in a Norwegian cohort. Author(s): Furberg AS, Thune I. Source: International Journal of Cancer. Journal International Du Cancer. 2003 May 10; 104(6): 669-76. Erratum In: Int J Cancer. 2003 May 10; 104(6): 799. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640672&dopt=Abstract
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Microalbuminuria and hypertension with focus on type 1 and type 2 diabetes. Author(s): Mogensen CE. Source: Journal of Internal Medicine. 2003 July; 254(1): 45-66. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823642&dopt=Abstract
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Microalbuminuria in hypertension. Author(s): Palatini P. Source: Current Hypertension Reports. 2003 June; 5(3): 208-14. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724052&dopt=Abstract
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Microalbuminuria is closely related to impaired arterial elasticity in untreated patients with essential hypertension. Author(s): Tsioufis C, Tzioumis C, Marinakis N, Toutouzas K, Tousoulis D, Kallikazaros I, Stefanadis C, Toutouzas P. Source: Nephron. Clinical Practice [electronic Resource]. 2003; 93(3): C106-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660419&dopt=Abstract
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Midtrimester triple-test levels in women with chronic hypertension and altered renal function. Author(s): Shenhav S, Gemer O, Sherman DJ, Peled R, Segal S. Source: Prenatal Diagnosis. 2003 February; 23(2): 166-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12575027&dopt=Abstract
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Might losartan reduce sudden cardiac death in diabetic patients with hypertension? Author(s): Aronow WS. Source: Lancet. 2003 August 23; 362(9384): 591-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12944056&dopt=Abstract
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Mild renal dysfunction and subclinical cardiovascular damage in primary hypertension. Author(s): Leoncini G, Viazzi F, Parodi D, Vettoretti S, Ratto E, Ravera M, Tomolillo C, Del Sette M, Bezante GP, Deferrari G, Pontremoli R. Source: Hypertension. 2003 July; 42(1): 14-8. Epub 2003 May 19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756221&dopt=Abstract
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Moderate-term effect of epoprostenol on severe portopulmonary hypertension. Author(s): Kato H, Katori T, Nakamura Y, Kawarasaki H. Source: Pediatric Cardiology. 2003 January-February; 24(1): 50-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574979&dopt=Abstract
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Modified endoscopic optic nerve decompression in idiopathic intracranial hypertension. Author(s): Gupta AK, Ganth MG, Gupta A. Source: The Journal of Laryngology and Otology. 2003 June; 117(6): 501-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12818064&dopt=Abstract
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Multicenter, open-label evaluation of hyperemia associated with use of bimatoprost in adults with open-angle glaucoma or ocular hypertension. Author(s): Abelson MB, Mroz M, Rosner SA, Dirks MS, Hirabayashi D. Source: Adv Ther. 2003 January-February; 20(1): 1-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12772813&dopt=Abstract
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Multiple actions of angiotensin II in hypertension: benefits of AT1 receptor blockade. Author(s): Schiffrin EL, Touyz RM. Source: Journal of the American College of Cardiology. 2003 September 3; 42(5): 911-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12957442&dopt=Abstract
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Myocardial ultrasonic backscatter in hypertension: relation to aldosterone and endothelin. Author(s): Kozakova M, Buralli S, Palombo C, Bernini G, Moretti A, Favilla S, Taddei S, Salvetti A. Source: Hypertension. 2003 February; 41(2): 230-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574087&dopt=Abstract
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Negative regulators of sodium transport in the kidney: key factors in understanding salt-sensitive hypertension? Author(s): Rossier BC. Source: The Journal of Clinical Investigation. 2003 April; 111(7): 947-50. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671041&dopt=Abstract
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Nephron number and primary hypertension. Author(s): Querfeld U, Niaudet P. Source: The New England Journal of Medicine. 2003 April 24; 348(17): 1717-9; Author Reply 1717-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713000&dopt=Abstract
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Nephron number and primary hypertension. Author(s): O'Neill WC. Source: The New England Journal of Medicine. 2003 April 24; 348(17): 1717-9; Author Reply 1717-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12712999&dopt=Abstract
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Nephron number and primary hypertension. Author(s): Johnson RJ, Rodriguez-Iturbe B, Herrera-Acosta J. Source: The New England Journal of Medicine. 2003 April 24; 348(17): 1717-9; Author Reply 1717-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711751&dopt=Abstract
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Nephron number in patients with primary hypertension. Author(s): Keller G, Zimmer G, Mall G, Ritz E, Amann K. Source: The New England Journal of Medicine. 2003 January 9; 348(2): 101-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519920&dopt=Abstract
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Nephrotic proteinuria as a result of essential hypertension. Author(s): Obialo CI, Hewan-Lowe K, Fulong B. Source: Kidney & Blood Pressure Research. 2002; 25(4): 250-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12424428&dopt=Abstract
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Neurovascular compression associated with trigeminal neuralgia and systemic arterial hypertension: surgical treatment. Author(s): Sendeski M, Aguiar PH, Zanetti MV, Teixeira MJ, Cescato VA. Source: Stereotactic and Functional Neurosurgery. 2002; 79(3-4): 284-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890987&dopt=Abstract
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New developments in the treatment of hypertension: are some antihypertensives more equal than others? Author(s): Gansevoort RT, Gans RO. Source: The Netherlands Journal of Medicine. 2003 May; 61(5 Suppl): 13-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12918545&dopt=Abstract
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Nicardipine to control neonatal hypertension during extracorporeal membrane oxygen support. Author(s): McBride BF, White CM, Campbell M, Frey BM. Source: The Annals of Pharmacotherapy. 2003 May; 37(5): 667-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12708943&dopt=Abstract
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Nitric oxide and portal hypertension. Author(s): Gonzalez-Abraldes J, Garcia-Pagan JC, Bosch J. Source: Metabolic Brain Disease. 2002 December; 17(4): 311-24. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12602508&dopt=Abstract
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Nitric oxide, cholesterol oxides and endothelium-dependent vasodilation in plasma of patients with essential hypertension. Author(s): Moriel P, Sevanian A, Ajzen S, Zanella MT, Plavnik FL, Rubbo H, Abdalla DS. Source: Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Medicas E Biologicas / Sociedade Brasileira De Biofisica . [et Al.]. 2002 November; 35(11): 1301-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12426629&dopt=Abstract
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No evidence that panic attacks are associated with the white coat effect in hypertension. Author(s): Davies SJ, Jackson PR, Ramsay LE, Ghahramani P, Palmer RL, Hippisley-Cox J. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 March-April; 5(2): 145-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671328&dopt=Abstract
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Nonfunctioning islet cell tumor presenting with ascites and portal hypertension. Author(s): Dalvi AN, Rege SA, Bapat MR, Abraham P, Joshi AS, Bapat RD. Source: Indian J Gastroenterol. 2002 November-December; 21(6): 227-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12546175&dopt=Abstract
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Noninvasive delivery of inhaled nitric oxide therapy for late pulmonary hypertension in newborn infants with congenital diaphragmatic hernia. Author(s): Kinsella JP, Parker TA, Ivy DD, Abman SH. Source: The Journal of Pediatrics. 2003 April; 142(4): 397-401. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12712057&dopt=Abstract
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Noninvasive study of endothelial function in white coat hypertension. Author(s): Gomez-Cerezo J, Rios Blanco JJ, Suarez Garcia I, Moreno Anaya P, Garcia Raya P, Vazquez-Munoz E, Barbado Hernandez FJ. Source: Hypertension. 2002 September; 40(3): 304-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12215471&dopt=Abstract
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Nonnarcotic analgesic use and the risk of hypertension in US women. Author(s): Dedier J, Stampfer MJ, Hankinson SE, Willett WC, Speizer FE, Curhan GC. Source: Hypertension. 2002 November; 40(5): 604-8; Discussion 601-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12411450&dopt=Abstract
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Non-pharmacological treatment of hypertension in primary health care: a 2-year open randomized controlled trial of lifestyle intervention against hypertension in eastern Finland. Author(s): Kastarinen MJ, Puska PM, Korhonen MH, Mustonen JN, Salomaa VV, Sundvall JE, Tuomilehto JO, Uusitupa MI, Nissinen AM; LIHEF Study Group. Source: Journal of Hypertension. 2002 December; 20(12): 2505-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12473876&dopt=Abstract
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Non-pharmacological treatment of hypertension in women. Author(s): Costa FV. Source: Journal of Hypertension. 2002 May; 20 Suppl 2: S57-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12183854&dopt=Abstract
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Nonselective beta-blockers plus nitrates in portal hypertension: an open question. Author(s): Merkel C. Source: Hepatology (Baltimore, Md.). 2003 June; 37(6): 1254-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12774001&dopt=Abstract
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Not so benign intracranial hypertension. Author(s): Digre KB. Source: Bmj (Clinical Research Ed.). 2003 March 22; 326(7390): 613-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649214&dopt=Abstract
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NSAIDs and hypertension. Author(s): Aisen PS, Schafer K, Grundman M, Thomas R, Thal LJ. Source: Archives of Internal Medicine. 2003 May 12; 163(9): 1115; Author Reply 1115-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742818&dopt=Abstract
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Nurse-recorded and ambulatory blood pressure predicts treatment-induced reduction of left ventricular hypertrophy equally well in hypertension: results from the Swedish irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA) study. Author(s): Nystrom F, Malmqvist K, Ohman KP, Kahan T. Source: Journal of Hypertension. 2002 August; 20(8): 1527-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12172314&dopt=Abstract
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Nutritional supplementation with Chlorella pyrenoidosa for mild to moderate hypertension. Author(s): Merchant RE, Andre CA, Sica DA. Source: Journal of Medicinal Food. 2002 Fall; 5(3): 141-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495586&dopt=Abstract
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Obesity hypertension in children: a problem of epidemic proportions. Author(s): Sorof J, Daniels S. Source: Hypertension. 2002 October; 40(4): 441-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12364344&dopt=Abstract
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Obesity, diabetes, hypertension, and vegetarian status among Seventh-Day Adventists in Barbados: preliminary results. Author(s): Brathwaite N, Fraser HS, Modeste N, Broome H, King R. Source: Ethn Dis. 2003 Winter; 13(1): 34-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723010&dopt=Abstract
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Obesity, hypertension, and insulin resistance. Author(s): Bloomgarden ZT. Source: Diabetes Care. 2002 November; 25(11): 2088-97. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401761&dopt=Abstract
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Obesity, insulin resistance, diabetes, and cardiovascular risk in children: an American Heart Association scientific statement from the Atherosclerosis, Hypertension, and Obesity in the Young Committee (Council on Cardiovascular Disease in the Young) and the Diabetes Committee (Council on Nutrition, Physical Activity, and Metabolism). Author(s): Steinberger J, Daniels SR; American Heart Association Atherosclerosis, Hypertension, and Obesity in the Young Committee (Council on Cardiovascular Disease in the Young); American Heart Association Diabetes Committee (Council on Nutrition, Physical Activity, and Metabolism). Source: Circulation. 2003 March 18; 107(10): 1448-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12642369&dopt=Abstract
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Obstructive jaundice in a case of portal hypertension. Author(s): Chawla A, Maheshwari M, Parmar H. Source: The British Journal of Radiology. 2003 September; 76(909): 667-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14500285&dopt=Abstract
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Obstructive sleep apnea syndrome: its relationship with hypertension. Author(s): Krieger AC, Redeker NS. Source: The Journal of Cardiovascular Nursing. 2002 October; 17(1): 1-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12358089&dopt=Abstract
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Ocular flutter in a patient with intracranial hypertension following cerebral venous thrombosis. Author(s): Shetty T. Source: Neurology. 2003 February 11; 60(3): 525; Author Reply 525. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12578949&dopt=Abstract
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Ocular flutter in a patient with intracranial hypertension following cerebral venous thrombosis. Author(s): Ploner CJ, Kupsch A. Source: Neurology. 2002 September 24; 59(6): 959. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12297595&dopt=Abstract
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Ocular Hypertension Treatment Study (OHTS) commentary. Author(s): Lee BL, Wilson MR; Ocular Hypertension Treatment Study (OHTS). Source: Current Opinion in Ophthalmology. 2003 April; 14(2): 74-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12698045&dopt=Abstract
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Ocular hypertension treatment study results could be misconstrued. Author(s): Weene LE. Source: Archives of Ophthalmology. 2003 July; 121(7): 1070; Author Reply 1070. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860828&dopt=Abstract
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Omapatrilat: still a promise in salt-sensitive hypertension? Author(s): Tojo A, Fujita T, Wilcox CS. Source: Journal of Hypertension. 2003 January; 21(1): 31-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12544430&dopt=Abstract
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One-year, randomized study comparing bimatoprost and timolol in glaucoma and ocular hypertension. Author(s): Higginbotham EJ, Schuman JS, Goldberg I, Gross RL, VanDenburgh AM, Chen K, Whitcup SM; Bimatoprost Study Groups 1 and 2. Source: Archives of Ophthalmology. 2002 October; 120(10): 1286-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12365906&dopt=Abstract
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Ophthalmic features of idiopathic intracranial hypertension. Author(s): Hung HL, Kao LY, Huang CC. Source: Eye (London, England). 2003 August; 17(6): 793-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928704&dopt=Abstract
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Optimal treatment of hypertension and cardiovascular risk reduction in African Americans: treatment approaches for outpatients. Author(s): Wright JT Jr, Douglas J. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 January-February; 5(1 Suppl 1): 18-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12556669&dopt=Abstract
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Optimal treatment of hypertension in African Americans. Reaching and maintaining target blood pressure goals. Author(s): Bakris GL, Ferdinand KC, Douglas JG, Sowers JR. Source: Postgraduate Medicine. 2002 October; 112(4): 73-4, 77-80, 83-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400150&dopt=Abstract
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Oral beta-blockers for mild to moderate hypertension during pregnancy. Author(s): Magee LA, Duley L. Source: Cochrane Database Syst Rev. 2003; (3): Cd002863. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917933&dopt=Abstract
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Oral L-arginine improves endothelial dysfunction in patients with essential hypertension. Author(s): Lekakis JP, Papathanassiou S, Papaioannou TG, Papamichael CM, Zakopoulos N, Kotsis V, Dagre AG, Stamatelopoulos K, Protogerou A, Stamatelopoulos SF. Source: International Journal of Cardiology. 2002 December; 86(2-3): 317-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12419572&dopt=Abstract
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Oral sildenafil as long-term adjunct therapy to inhaled iloprost in severe pulmonary arterial hypertension. Author(s): Ghofrani HA, Rose F, Schermuly RT, Olschewski H, Wiedemann R, Kreckel A, Weissmann N, Ghofrani S, Enke B, Seeger W, Grimminger F. Source: Journal of the American College of Cardiology. 2003 July 2; 42(1): 158-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12849677&dopt=Abstract
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Orlistat improves blood pressure control in obese subjects with treated but inadequately controlled hypertension. Author(s): Bakris G, Calhoun D, Egan B, Hellmann C, Dolker M, Kingma I; orlistat and resistant hypertension investigators. Source: Journal of Hypertension. 2002 November; 20(11): 2257-67. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12409965&dopt=Abstract
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Orthodeoxia without platypnea from interatrial defect associated with persistent left superior vena cava in the absence of pulmonary hypertension. Author(s): Maniscalco M, Dialetto G, Tufano G, Romano A, Sofia M. Source: Respiration; International Review of Thoracic Diseases. 2003 March-April; 70(2): 207-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740520&dopt=Abstract
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Osteopathic manipulative medicine in the treatment of hypertension: an alternative, conventional approach. Author(s): Spiegel AJ, Capobianco JD, Kruger A, Spinner WD. Source: Heart Disease. 2003 July-August; 5(4): 272-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12877760&dopt=Abstract
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Outcome in 91 consecutive patients with pulmonary arterial hypertension receiving epoprostenol. Author(s): Kuhn KP, Byrne DW, Arbogast PG, Doyle TP, Loyd JE, Robbins IM. Source: American Journal of Respiratory and Critical Care Medicine. 2003 February 15; 167(4): 580-6. Epub 2002 November 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446266&dopt=Abstract
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Outcomes of treating hypertension in the elderly: a short commentary on current issues. Author(s): Weber MA. Source: The American Journal of Geriatric Cardiology. 2003 January-February; 12(1): 148. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12502910&dopt=Abstract
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Outcomes with nifedipine GITS or Co-amilozide in hypertensive diabetics and nondiabetics in Intervention as a Goal in Hypertension (INSIGHT). Author(s): Mancia G, Brown M, Castaigne A, de Leeuw P, Palmer CR, Rosenthal T, Wagener G, Ruilope LM; INSIGHT. Source: Hypertension. 2003 March; 41(3): 431-6. Epub 2003 February 17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623939&dopt=Abstract
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Overestimation of pulmonary artery occlusion pressure in pulmonary hypertension due to partial occlusion. Author(s): Leatherman JW, Shapiro RS. Source: Critical Care Medicine. 2003 January; 31(1): 93-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12545000&dopt=Abstract
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Oxidant stress in pre-eclampsia and essential hypertension. Author(s): Kumar CA, Das UN. Source: J Assoc Physicians India. 2002 November; 50: 1372-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12583464&dopt=Abstract
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Oxidative stress in juvenile essential hypertension. Author(s): Turi S, Friedman A, Bereczki C, Papp F, Kovacs J, Karg E, Nemeth I. Source: Journal of Hypertension. 2003 January; 21(1): 145-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12544446&dopt=Abstract
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Oxidative stress in kidney transplant patients with calcineurin inhibitor-induced hypertension: effect of ramipril. Author(s): Calo LA, Davis PA, Giacon B, Pagnin E, Sartori M, Riegler P, Antonello A, Huber W, Semplicini A. Source: Journal of Cardiovascular Pharmacology. 2002 October; 40(4): 625-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12352326&dopt=Abstract
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Oxidative stress in patients with primary pulmonary hypertension. Author(s): Irodova NL, Lankin VZ, Konovalova GK, Kochetov AG, Chazova IE. Source: Bulletin of Experimental Biology and Medicine. 2002 June; 133(6): 580-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12447471&dopt=Abstract
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Oxygen-15 positron-emission tomography for predicting selective delivery of a chemotherapeutic agent to hepatic cancers during angiotensin II-induced hypertension. Author(s): Koh T, Taniguchi H, Yamagishi H. Source: Cancer Chemotherapy and Pharmacology. 2003 April; 51(4): 349-58. Epub 2003 March 05. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12721763&dopt=Abstract
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Pathogenesis and consequences of essential hypertension. Author(s): Rao MS. Source: J Indian Med Assoc. 2003 April; 101(4): 251-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12964644&dopt=Abstract
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Pathological lesions causing pulmonary hypertension after closure of a ventricular septal defect. Author(s): Maeda K, Yamaki S, Nishiyama M, Murakami Y, Takahashi Y, Takamoto S. Source: Jpn J Thorac Cardiovasc Surg. 2003 September; 51(9): 430-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14529159&dopt=Abstract
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Pathophysiological insights from a case of reversible pulmonary arterial hypertension. Author(s): Mukerjee D, Kingdon E, Vanderpump M, Coghlan JG. Source: Journal of the Royal Society of Medicine. 2003 August; 96(8): 403-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12893860&dopt=Abstract
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Patient knowledge and awareness of hypertension is suboptimal: results from a large health maintenance organization. Author(s): Alexander M, Gordon NP, Davis CC, Chen RS. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 July-August; 5(4): 254-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939565&dopt=Abstract
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Pharmacological modulation of platelet function in hypertension. Author(s): Blann AD, Nadar S, Lip GY. Source: Hypertension. 2003 July; 42(1): 1-7. Epub 2003 June 02. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12782643&dopt=Abstract
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Pharmacological rationale for the use of somatostatin and analogues in portal hypertension. Author(s): Reynaert H, Geerts A. Source: Alimentary Pharmacology & Therapeutics. 2003 August 15; 18(4): 375-86. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12940922&dopt=Abstract
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Plasma homocysteine levels in Indian patients with essential hypertension and their siblings. Author(s): Jain S, Ram H, Kumari S, Khullar M. Source: Renal Failure. 2003 March; 25(2): 195-201. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12739826&dopt=Abstract
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Polymorphism in the promoter region of the insulin-like growth factor I gene is related to carotid intima-media thickness and aortic pulse wave velocity in subjects with hypertension. Author(s): Schut AF, Janssen JA, Deinum J, Vergeer JM, Hofman A, Lamberts SW, Oostra BA, Pols HA, Witteman JC, van Duijn CM. Source: Stroke; a Journal of Cerebral Circulation. 2003 July; 34(7): 1623-7. Epub 2003 June 05. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791939&dopt=Abstract
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Portopulmonary hypertension in decompensated cirrhosis with refractory ascites. Author(s): Benjaminov FS, Prentice M, Sniderman KW, Siu S, Liu P, Wong F. Source: Gut. 2003 September; 52(9): 1355-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912870&dopt=Abstract
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Portopulmonary hypertension: an increasingly important complication of cirrhosis. Author(s): Blendis L, Wong F. Source: Gastroenterology. 2003 August; 125(2): 622-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12891571&dopt=Abstract
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Positional change in blood pressure and 8-year risk of hypertension: the CARDIA Study. Author(s): Thomas RJ, Liu K, Jacobs DR Jr, Bild DE, Kiefe CI, Hulley SB. Source: Mayo Clinic Proceedings. 2003 August; 78(8): 951-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12911043&dopt=Abstract
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Potential causes of secondary hypertension. Author(s): Schapera CH. Source: American Family Physician. 2003 July 1; 68(1): 42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12887112&dopt=Abstract
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Preliminary characterisation of the promoter of the human p22(phox) gene: identification of a new polymorphism associated with hypertension. Author(s): Moreno MU, San Jose G, Orbe J, Paramo JA, Beloqui O, Diez J, Zalba G. Source: Febs Letters. 2003 May 8; 542(1-3): 27-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12729892&dopt=Abstract
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Prevalence, treatment, and control of hypertension in chronic hemodialysis patients in the United States. Author(s): Agarwal R, Nissenson AR, Batlle D, Coyne DW, Trout JR, Warnock DG. Source: The American Journal of Medicine. 2003 September; 115(4): 291-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12967694&dopt=Abstract
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Preventing heart disease by controlling hypertension: impact of hypertensive subtype, stage, age, and sex. Author(s): Wong ND, Thakral G, Franklin SS, L'Italien GJ, Jacobs MJ, Whyte JL, Lapuerta P. Source: American Heart Journal. 2003 May; 145(5): 888-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12766749&dopt=Abstract
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Prevention of hypertension and its complications: theoretical basis and guidelines for treatment. Author(s): Flack JM, Peters R, Shafi T, Alrefai H, Nasser SA, Crook E. Source: Journal of the American Society of Nephrology : Jasn. 2003 July; 14(7 Suppl 2): S92-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12819310&dopt=Abstract
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Primary hypertension-induced cerebellar encephalopathy causing obstructive hydrocephalus. Case report. Author(s): Verrees M, Fernandes Filho JA, Suarez JI, Ratcheson RA. Source: Journal of Neurosurgery. 2003 June; 98(6): 1307-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816279&dopt=Abstract
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Primary pulmonary hypertension may be a heterogeneous disease with a second locus on chromosome 2q31. Author(s): Rindermann M, Grunig E, von Hippel A, Koehler R, Miltenberger-Miltenyi G, Mereles D, Arnold K, Pauciulo M, Nichols W, Olschewski H, Hoeper MM, Winkler J, Katus HA, Kubler W, Bartram CR, Janssen B. Source: Journal of the American College of Cardiology. 2003 June 18; 41(12): 2237-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12821254&dopt=Abstract
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Primary pulmonary hypertension. Author(s): Runo JR, Loyd JE. Source: Lancet. 2003 May 3; 361(9368): 1533-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12737878&dopt=Abstract
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Progression of uncontrolled hypertension and implications for managing its sequelae. Author(s): Kannel WB. Source: Manag Care. 2003 August; 12(8 Suppl Hypertension): 26-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12971590&dopt=Abstract
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Proximal pulmonary arterial and intrapulmonary radiologic features of Eisenmenger syndrome and primary pulmonary hypertension. Author(s): Perloff JK, Hart EM, Greaves SM, Miner PD, Child JS. Source: The American Journal of Cardiology. 2003 July 15; 92(2): 182-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860221&dopt=Abstract
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Psychosocial factors and risk of hypertension: the Coronary Artery Risk Development in Young Adults (CARDIA) study. Author(s): Yan LL, Liu K, Matthews KA, Daviglus ML, Ferguson TF, Kiefe CI. Source: Jama : the Journal of the American Medical Association. 2003 October 22; 290(16): 2138-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14570949&dopt=Abstract
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Pulmonary arterial hypertension in previously splenectomized patients with betathalassemic disorders. Author(s): Atichartakarn V, Likittanasombat K, Chuncharunee S, Chandanamattha P, Worapongpaiboon S, Angchaisuksiri P, Aryurachai K. Source: International Journal of Hematology. 2003 August; 78(2): 139-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12953808&dopt=Abstract
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Pulmonary arterial hypertension--the primary pulmonary hypertension syndromes. Author(s): Hey JC, Scharf SM. Source: Isr Med Assoc J. 2003 April; 5(4): 298-303. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14509142&dopt=Abstract
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Pulmonary hypertension in patients with end-stage renal disease. Author(s): Yigla M, Nakhoul F, Sabag A, Tov N, Gorevich B, Abassi Z, Reisner SA. Source: Chest. 2003 May; 123(5): 1577-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740276&dopt=Abstract
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Pulmonary hypertension in pregnancy. Author(s): Kelley SE. Source: J Ark Med Soc. 2000 September; 97(3): 98-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12876809&dopt=Abstract
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Pulmonary hypertension in systemic sclerosis. Author(s): Denton CP, Black CM. Source: Rheumatic Diseases Clinics of North America. 2003 May; 29(2): 335-49, Vii. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841298&dopt=Abstract
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Pulmonary hypertension in the setting of acquired systemic arteriovenous fistulas. Author(s): Bhatia S, Morrison JF, Bower TC, McGoon MD. Source: Mayo Clinic Proceedings. 2003 July; 78(7): 908-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839088&dopt=Abstract
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Pulmonary hypertension: new perspectives. Author(s): Nauser TD, Stites SW. Source: Congestive Heart Failure (Greenwich, Conn.). 2003 May-June; 9(3): 155-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826774&dopt=Abstract
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Pulmonary venous flow in pure mitral stenosis and sinus rhythm--does pulmonary hypertension alter pulmonary venous flow velocity? Author(s): Ha JW, Chung N, Goh CW, Jang KJ, Kang SM, Rim SJ, Jang Y, Shim WH, Cho SY, Kim SS. Source: Echocardiography (Mount Kisco, N.Y.). 2003 February; 20(2): 129-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12848677&dopt=Abstract
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Quality control of the blood pressure phenotype in the European Project on Genes in Hypertension. Author(s): Kuznetsova T, Staessen JA, Kawecka-Jaszcz K, Babeanu S, Casiglia E, Filipovsky J, Nachev C, Nikitin Y, Peleska J, O'Brien E. Source: Blood Pressure Monitoring. 2002 August; 7(4): 215-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12198337&dopt=Abstract
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Quality of hypertension treatment and risk of stroke in the general population. Author(s): Klungel OH. Source: Journal of Hypertension. 2002 October; 20(10): 1949-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12359971&dopt=Abstract
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Quality of life on randomized treatment for isolated systolic hypertension: results from the Syst-Eur Trial. Author(s): Fletcher AE, Bulpitt CJ, Thijs L, Tuomilehto J, Antikainen R, Bossini A, Browne J, Duggan J, Kawecka-Jaszcz K, Kivinen P, Sarti C, Terzoli L, Staessen JA; SystEur Trial Investigators. Source: Journal of Hypertension. 2002 October; 20(10): 2069-79. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12359987&dopt=Abstract
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Quantitative relationship between severity of pulmonary hypertension and LV diastolic function has been established. Author(s): Barasch E, Moustapha A, Kaushik V, Diaz S, Kang SH. Source: Journal of the American College of Cardiology. 2003 March 19; 41(6): 1066; Author Reply 1066-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12651061&dopt=Abstract
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Questioning race-based hypertension management. Author(s): Denberg TD. Source: Archives of Internal Medicine. 2003 July 28; 163(14): 1744-5; Author Reply 1745. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885694&dopt=Abstract
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Questions remain regarding patients with aortic stenosis and severe pulmonary hypertension. Author(s): Rahimtoola SH. Source: Journal of the American College of Cardiology. 2003 May 21; 41(10): 1847-8; Author Reply 1848. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767677&dopt=Abstract
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QUICKI is a useful index of insulin sensitivity in subjects with hypertension. Author(s): Chen H, Sullivan G, Yue LQ, Katz A, Quon MJ. Source: American Journal of Physiology. Endocrinology and Metabolism. 2003 April; 284(4): E804-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678026&dopt=Abstract
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Randomized clinical trial comparing intraocular pressure-lowering efficacy of bimatoprost and latanoprost in patients with ocular hypertension or glaucoma. Author(s): Eisenberg D. Source: American Journal of Ophthalmology. 2003 July; 136(1): 217; Author Reply 217-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12834708&dopt=Abstract
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Randomized, comparative, double-blind study of amlodipine vs. nicardipine as a treatment of isolated systolic hypertension in the elderly. Author(s): Mounier-Vehier C, Jaboureck O, Emeriau JP, Bernaud C, Clerson P, Carre A. Source: Fundamental & Clinical Pharmacology. 2002 December; 16(6): 537-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12685513&dopt=Abstract
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Reduced activity of the kallikrein-kinin system predominates over renin-angiotensin system overactivity in all conditions of sodium balance in essential hypertensives and family-related hypertension. Author(s): Sanchez R, Nolly H, Giannone C, Baglivo HP, Ramirez AJ. Source: Journal of Hypertension. 2003 February; 21(2): 411-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12569273&dopt=Abstract
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Reduced heart rate variability in hypertension: associations with lifestyle factors and plasma renin activity. Author(s): Virtanen R, Jula A, Kuusela T, Helenius H, Voipio-Pulkki LM. Source: Journal of Human Hypertension. 2003 March; 17(3): 171-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12624607&dopt=Abstract
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Refractory hypertension and sleep apnoea: effect of CPAP on blood pressure and baroreflex. Author(s): Logan AG, Tkacova R, Perlikowski SM, Leung RS, Tisler A, Floras JS, Bradley TD. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 February; 21(2): 241-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12608436&dopt=Abstract
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Refractory hypertension: recognition of psychiatric comorbidity. Author(s): Handler J. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 May-June; 5(3): 235-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826793&dopt=Abstract
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Regression of electrocardiographic left ventricular hypertrophy by losartan versus atenolol: The Losartan Intervention for Endpoint reduction in Hypertension (LIFE) Study. Author(s): Okin PM, Devereux RB, Jern S, Kjeldsen SE, Julius S, Nieminen MS, Snapinn S, Harris KE, Aurup P, Edelman JM, Dahlof B; Losartan Intervention for Endpoint reduction in hypertension Study Investigations. Source: Circulation. 2003 August 12; 108(6): 684-90. Epub 2003 July 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885747&dopt=Abstract
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Regression of left ventricular hypertrophy after treatment of hypertension: comparison of directed M-echocardiography with magnetic resonance imaging in quantification of serial mass changes. Author(s): Tse HF, Cheung BM, Ng W, Chan JK, Devereux RB, Lau CP. Source: Journal of Cardiac Failure. 2003 April; 9(2): 122-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12751133&dopt=Abstract
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Relation of C-reactive protein and fibrinogen to coronary artery calcium in subjects with systemic hypertension. Author(s): Kullo IJ, McConnell JP, Bailey KR, Kardia SL, Bielak LF, Peyser PA, Sheedy PF 2nd, Boerwinkle E, Turner ST. Source: The American Journal of Cardiology. 2003 July 1; 92(1): 56-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12842247&dopt=Abstract
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Relationship between eicosanoids and endothelin-1 in the pathogenesis of erythropoietin-induced hypertension in uremic rats. Author(s): Rodrigue ME, Moreau C, Lariviere R, Lebel M. Source: Journal of Cardiovascular Pharmacology. 2003 March; 41(3): 388-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12605017&dopt=Abstract
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Relationship between visceral fat accumulation and hypertension in obese men. Author(s): Watanabe J, Tochikubo O. Source: Clinical and Experimental Hypertension (New York, N.Y. : 1993). 2003 April; 25(3): 199-208. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716082&dopt=Abstract
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Relationship of light to moderate alcohol consumption and risk of hypertension in Japanese male office workers. Author(s): Nakanishi N, Makino K, Nishina K, Suzuki K, Tatara K. Source: Alcoholism, Clinical and Experimental Research. 2002 July; 26(7): 988-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12170108&dopt=Abstract
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Relationship of urinary sodium/potassium excretion and calcium intake to blood pressure and prevalence of hypertension among older Chinese vegetarians. Author(s): Kwok TC, Chan TY, Woo J. Source: European Journal of Clinical Nutrition. 2003 February; 57(2): 299-304. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571663&dopt=Abstract
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Relevance of the plasma renin hormonal control system that regulates blood pressure and sodium balance for correctly treating hypertension and for evaluating ALLHAT. Author(s): Laragh JH, Sealey JE. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2003 May; 16(5 Pt 1): 407-15. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745204&dopt=Abstract
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Renal and cardiovascular responses to water immersion in essential hypertension: is there a role for the opioidergic system? Author(s): Coruzzi P, Parati G, Brambilla L, Brambilla V, Gualerzi M, Novarini A, Mancia G, Castiglioni P, Di Rienzo M. Source: Nephron. Physiology [electronic Resource]. 2003; 94(3): P51-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902616&dopt=Abstract
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Renal sodium retention in portal hypertension and hepatorenal reflex: from practice to science. Author(s): Jimenez-Saenz M, Soria IC, Bernardez JR, Gutierrez JM. Source: Hepatology (Baltimore, Md.). 2003 June; 37(6): 1494; Author Reply 1494-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12774029&dopt=Abstract
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Renin-angiotensin gene polymorphism in children with uremia and essential hypertension. Author(s): Papp F, Friedman AL, Bereczki C, Haszon I, Kiss E, Endreffy E, Turi S. Source: Pediatric Nephrology (Berlin, Germany). 2003 February; 18(2): 150-4. Epub 2002 December 18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12579405&dopt=Abstract
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Renin-angiotensin-aldosterone system and G-protein beta-3 subunit gene polymorphisms in salt-sensitive essential hypertension. Author(s): Pamies-Andreu E, Ramirez-Lorca R, Stiefel Garcia-Junco P, Muniz-Grijalbo O, Vallejo-Maroto I, Garcia Morillo S, Miranda-Guisado ML, Ortiz JV, Carneado de la Fuente J. Source: Journal of Human Hypertension. 2003 March; 17(3): 187-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12624609&dopt=Abstract
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Renin-angiotensin-aldosterone system loci and multilocus interactions in youngonset essential hypertension. Author(s): Porto PI, Garcia SI, Dieuzeide G, Gonzalez C, Pirola CJ. Source: Clinical and Experimental Hypertension (New York, N.Y. : 1993). 2003 February; 25(2): 117-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12611423&dopt=Abstract
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Renovascular hypertension secondary to spontaneous renal artery dissection and treatment with stenting. Author(s): Bilge AK, Nisanci Y, Yilmaz E, Umman B, Hunerel D, Ozsaruhan O. Source: Int J Clin Pract. 2003 June; 57(5): 435-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846352&dopt=Abstract
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Research into policy. Hypertension and diabetes mellitus in the Caribbean. Author(s): Forrester TE. Source: The West Indian Medical Journal. 2003 June; 52(2): 164-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12974071&dopt=Abstract
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Response of the right ventricle to acute pulmonary vasodilation predicts the outcome in patients with advanced heart failure and pulmonary hypertension. Author(s): Gavazzi A, Ghio S, Scelsi L, Campana C, Klersy C, Serio A, Raineri C, Tavazzi L. Source: American Heart Journal. 2003 February; 145(2): 310-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595849&dopt=Abstract
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Response to travoprost in black and nonblack patients with open-angle glaucoma or ocular hypertension. Author(s): Netland PA, Robertson SM, Sullivan EK, Silver L, Bergamini MV, Krueger S, Weiner AL, Davis AA; Travoprost Study Groups. Source: Adv Ther. 2003 May-June; 20(3): 149-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12956257&dopt=Abstract
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Results of the betaxolol versus placebo treatment trial in ocular hypertension. Author(s): Kamal D, Garway-Heath D, Ruben S, O'Sullivan F, Bunce C, Viswanathan A, Franks W, Hitchings R. Source: Graefe's Archive for Clinical and Experimental Ophthalmology = Albrecht Von Graefes Archiv Fur Klinische Und Experimentelle Ophthalmologie. 2003 March; 241(3): 196-203. Epub 2003 February 19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12644943&dopt=Abstract
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Reversible pulmonary hypertension and thalidomide therapy for multiple myeloma. Author(s): Younis TH. Source: British Journal of Haematology. 2003 April; 121(1): 191-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12670354&dopt=Abstract
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Reversible segmental portal hypertension--an unusual presentation of abdominal tuberculosis in a renal transplant recipient. Author(s): Varma PP, Seth AK, Kumar RS. Source: J Assoc Physicians India. 2003 February; 51: 218-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12725273&dopt=Abstract
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Risk of hypertension among women in the EPIC-Potsdam Study: comparison of relative risk estimates for exploratory and hypothesis-oriented dietary patterns. Author(s): Schulze MB, Hoffmann K, Kroke A, Boeing H. Source: American Journal of Epidemiology. 2003 August 15; 158(4): 365-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915502&dopt=Abstract
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Role of endothelin-1 in hypertension. Author(s): Iglarz M, Schiffrin EL. Source: Current Hypertension Reports. 2003 April; 5(2): 144-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12642014&dopt=Abstract
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Role of kidney in hypertension. Author(s): Tripathi S, Tripathi K. Source: J Indian Med Assoc. 2003 April; 101(4): 260-2, 264-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12964647&dopt=Abstract
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Role of para-esophageal collateral veins in patients with portal hypertension based on the results of endoscopic ultrasonography and liver scintigraphy analysis. Author(s): Irisawa A, Obara K, Bhutani MS, Saito A, Shishido H, Shibukawa G, Takagi T, Yamamoto G, Seino O, Shishido F, Kasukawa R, Sato Y. Source: Journal of Gastroenterology and Hepatology. 2003 March; 18(3): 309-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12603532&dopt=Abstract
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Safety and efficacy of sibutramine in overweight Hispanic patients with hypertension. Author(s): Fanghanel G, Cortinas L, Sanchez-Reyes L, Gomez-Santos R, Campos-Franco E, Berber A. Source: Adv Ther. 2003 March-April; 20(2): 101-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12836810&dopt=Abstract
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Second International Symposium on Obesity and Hypertension: genetics and molecular mechanisms, 25-27 October 2001, Berlin, Germany. Author(s): Sharma AM. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 October; 26(10): 1283-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12355322&dopt=Abstract
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Self-reported stress and subsequent hospital admissions as a result of hypertension, varicose veins and haemorrhoids. Author(s): Metcalfe C, Davey Smith G, Macleod J, Heslop P, Hart C. Source: Journal of Public Health Medicine. 2003 March; 25(1): 62-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12669921&dopt=Abstract
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Serious perinatal complications of non-proteinuric hypertension: an international, multicentre, retrospective cohort study. Author(s): Magee LA, von Dadelszen P, Bohun CM, Rey E, El-Zibdeh M, Stalker S, Ross S, Hewson S, Logan AG, Ohlsson A, Naeem T, Thornton JG, Abdalla M, Walkinshaw S, Brown M, Davis G, Hannah ME. Source: J Obstet Gynaecol Can. 2003 May; 25(5): 372-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738978&dopt=Abstract
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Seventh report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7): resetting the hypertension sails. Author(s): Lenfant C, Chobanian AV, Jones DW, Roccella EJ; Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Source: Hypertension. 2003 June; 41(6): 1178-9. Epub 2003 May 19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756222&dopt=Abstract
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Severe acidosis in a patient with type 2 diabetes mellitus, hypertension, and renal failure. Author(s): Kumar A, Nugent K, Kalakunja A, Pirtle F. Source: Chest. 2003 May; 123(5): 1726-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740293&dopt=Abstract
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Severe portopulmonary hypertension in congenital hepatic fibrosis. Author(s): Hsu CM, Chiu CT, Lien JM, Ng KF. Source: Chang Gung Med J. 2003 March; 26(3): 193-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12790224&dopt=Abstract
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Severity of human hypertension in relation to the age in which high blood pressure makes its presumptive appearance. Author(s): Cugini P, Ferrari P, De Rosa R, Caliumi C, Delfini E, Colotto M, Fontana S, Mandolini C, Manetti L, Letizia C. Source: Clin Ter. 2003 January-February; 154(1): 21-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854280&dopt=Abstract
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Shifting trends in the pharmacologic treatment of hypertension in a Nigerian tertiary hospital: a real-world evaluation of the efficacy, safety, rationality and pharmacoeconomics of old and newer antihypertensive drugs. Author(s): Adigun AQ, Ishola DA, Akintomide AO, Ajayi AA. Source: Journal of Human Hypertension. 2003 April; 17(4): 277-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714973&dopt=Abstract
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Signaling molecules in pulmonary hypertension. Author(s): Hoeper MM. Source: The New England Journal of Medicine. 2003 May 22; 348(21): 2151; Author Reply 2151. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12761375&dopt=Abstract
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Sildenafil as a treatment for pulmonary hypertension. Author(s): Carroll WD, Dhillon R. Source: Archives of Disease in Childhood. 2003 September; 88(9): 827-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937112&dopt=Abstract
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Sildenafil for long-term treatment of nonoperable chronic thromboembolic pulmonary hypertension. Author(s): Ghofrani HA, Schermuly RT, Rose F, Wiedemann R, Kohstall MG, Kreckel A, Olschewski H, Weissmann N, Enke B, Ghofrani S, Seeger W, Grimminger F. Source: American Journal of Respiratory and Critical Care Medicine. 2003 April 15; 167(8): 1139-41. Epub 2003 January 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684251&dopt=Abstract
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Sildenafil for treatment of lung fibrosis and pulmonary hypertension: a randomised controlled trial. Author(s): Ghofrani HA, Wiedemann R, Rose F, Schermuly RT, Olschewski H, Weissmann N, Gunther A, Walmrath D, Seeger W, Grimminger F. Source: Lancet. 2002 September 21; 360(9337): 895-900. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12354470&dopt=Abstract
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Sildenafil in secondary pulmonary hypertension. Author(s): Cubillos-Garzon LA, Casas JP, Morillo CA. Source: International Journal of Cardiology. 2003 May; 89(1): 101-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727014&dopt=Abstract
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Sitaxsentan in pulmonary arterial hypertension. Author(s): Apostolopoulou SC, Rammos S. Source: Chest. 2003 May; 123(5): 1772; Author Reply 1772-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740304&dopt=Abstract
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Six-month randomized clinical trial comparing intraocular pressure-lowering efficacy of bimatoprost and latanoprost in patients with ocular hypertension or glaucoma. Author(s): Fellenbaum PS. Source: American Journal of Ophthalmology. 2003 August; 136(2): 392; Author Reply 392-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12888081&dopt=Abstract
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Small intestinal motility disturbances and bacterial overgrowth in patients with liver cirrhosis and portal hypertension. Author(s): Gunnarsdottir SA, Sadik R, Shev S, Simren M, Sjovall H, Stotzer PO, Abrahamsson H, Olsson R, Bjornsson ES. Source: The American Journal of Gastroenterology. 2003 June; 98(6): 1362-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12818282&dopt=Abstract
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Socioeconomic aspects of spousal concordance for hypertension, obesity, and smoking in a community of Rio de Janeiro, Brazil. Author(s): Bloch KV, Klein CH, de Souza e Silva NA, Nogueira Ada R, Salis LH. Source: Arquivos Brasileiros De Cardiologia. 2003 February; 80(2): 179-86, 171-8. Epub 2003 February 25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640511&dopt=Abstract
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Splicing mutation of the prostacyclin synthase gene in a family associated with hypertension. Author(s): Nakayama T, Soma M, Watanabe Y, Hasimu B, Kanmatsuse K, Kokubun S, Morrow JD, Oates JA. Source: Advances in Experimental Medicine and Biology. 2003; 525: 165-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12751759&dopt=Abstract
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Study design of HOMED-BP: hypertension objective treatment based on measurement by electrical devices of blood pressure. Author(s): Fujiwara T, Matsubara M, Ohkubo T, Imai Y. Source: Clinical and Experimental Hypertension (New York, N.Y. : 1993). 2003 April; 25(3): 143-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716076&dopt=Abstract
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Study finds hypertension incidence is rising. Author(s): Levenson D. Source: Rep Med Guidel Outcomes Res. 2003 July 25; 14(14): 1-2, 6-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12931696&dopt=Abstract
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Subjects with essential hypertension are more sensitive to the inhibition of 11 betaHSD by liquorice. Author(s): Sigurjonsdottir HA, Manhem K, Axelson M, Wallerstedt S. Source: Journal of Human Hypertension. 2003 February; 17(2): 125-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574791&dopt=Abstract
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Surgical and radiological management of renovascular hypertension in a developing country. Author(s): Kumar A, Dubey D, Bansal P, Sanjeevan KV, Gulati S, Jain S, Sharma K. Source: The Journal of Urology. 2003 September; 170(3): 727-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12913683&dopt=Abstract
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Susceptibility genes for hypertension and renal failure. Author(s): Freedman BI. Source: Journal of the American Society of Nephrology : Jasn. 2003 July; 14(7 Suppl 2): S192-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12819327&dopt=Abstract
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Symposium reporter 2003. New therapeutic options in the management of hypertension to heart failure. Orlando, Florida, USA, March 6, 2003. Author(s): Cohn JN, Velazquez EJ, Musher J. Source: Journal of the American Medical Directors Association. 2003; : 1-16, Quiz 17. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12924409&dopt=Abstract
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Symptomatic aortic stenosis: does systemic hypertension play an additional role? Author(s): Antonini-Canterin F, Huang G, Cervesato E, Faggiano P, Pavan D, Piazza R, Nicolosi GL. Source: Hypertension. 2003 June; 41(6): 1268-72. Epub 2003 April 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707297&dopt=Abstract
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Symptoms and the distress they cause: comparison of an aldosterone antagonist and a calcium channel blocking agent in patients with systolic hypertension. Author(s): Hollenberg NK, Williams GH, Anderson R, Akhras KS, Bittman RM, Krause SL. Source: Archives of Internal Medicine. 2003 July 14; 163(13): 1543-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860576&dopt=Abstract
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Systematic review of the prevention of delayed ischemic neurological deficits with hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage. Author(s): Treggiari MM, Walder B, Suter PM, Romand JA. Source: Journal of Neurosurgery. 2003 May; 98(5): 978-84. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744357&dopt=Abstract
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Systemic lupus erythematosus-associated pulmonary hypertension: good outcome following sildenafil therapy. Author(s): Molina J, Lucero E, Luluaga S, Bellomio V, Spindler A, Berman A. Source: Lupus. 2003; 12(4): 321-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12729058&dopt=Abstract
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Systolic hypertension in hemodialysis patients. Author(s): Agarwal R. Source: Seminars in Dialysis. 2003 May-June; 16(3): 208-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12753679&dopt=Abstract
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Targeting sources of superoxide and increasing nitric oxide bioavailability in hypertension. Author(s): Elmarakby AA, Williams JM, Pollock DM. Source: Curr Opin Investig Drugs. 2003 March; 4(3): 282-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12735229&dopt=Abstract
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The aggressive treatment of hypertension. Author(s): Ramanan SV. Source: Lancet. 2003 May 3; 361(9368): 1510. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12737860&dopt=Abstract
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The alteration of the pulmonary artery flow spectrum with pulmonary hypertension. Author(s): Guogan W, Baiping C, Hanying L, Rusheng C. Source: Chinese Medical Sciences Journal = Chung-Kuo I Hsueh K'o Hsueh Tsa Chih / Chinese Academy of Medical Sciences. 1999 December; 14(4): 220-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894895&dopt=Abstract
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The burden of uncontrolled hypertension: morbidity and mortality associated with disease progression. Author(s): Cushman WC. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 May-June; 5(3 Suppl 2): 14-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826766&dopt=Abstract
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The dilemma of immediate preoperative hypertension: to treat and operate, or to postpone surgery? Author(s): Weksler N, Klein M, Szendro G, Rozentsveig V, Schily M, Brill S, Tarnopolski A, Ovadia L, Gurman GM. Source: Journal of Clinical Anesthesia. 2003 May; 15(3): 179-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12770652&dopt=Abstract
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The economic impact of hypertension. Author(s): Elliott WJ. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 May-June; 5(3 Suppl 2): 3-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826765&dopt=Abstract
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The ethnic characteristics and prevalence of diabetes mellitus, hypertension and hyperlipidaemia in patients who underwent coronary artery bypass grafting in Hospital Universiti Kebangsaan Malaysia. Author(s): Chiam P, Abdullah F, Chow HK, Adeeb SM, Yousafzai MS. Source: Med J Malaysia. 2002 December; 57(4): 460-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12733171&dopt=Abstract
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The hypertension management program: identifying opportunities for improvement. Author(s): Maue SK, Jackson JH 4th, Weiss BA, Rivo ML, Jhaveri V, Lennert B. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 May-June; 5(3 Suppl 2): 33-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826768&dopt=Abstract
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The JNC 7 hypertension guidelines. Author(s): Phillips B. Source: Jama : the Journal of the American Medical Association. 2003 September 10; 290(10): 1314; Author Reply 1314-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966119&dopt=Abstract
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The JNC 7 hypertension guidelines. Author(s): Majernick TG, Madden N. Source: Jama : the Journal of the American Medical Association. 2003 September 10; 290(10): 1314; Author Reply 1314-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966118&dopt=Abstract
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The JNC 7 hypertension guidelines. Author(s): Murthy GD. Source: Jama : the Journal of the American Medical Association. 2003 September 10; 290(10): 1313; Author Reply 1314-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966117&dopt=Abstract
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The JNC 7 hypertension guidelines. Author(s): Brotman DJ, Frost SD. Source: Jama : the Journal of the American Medical Association. 2003 September 10; 290(10): 1313-4; Author Reply 1314-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966116&dopt=Abstract
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The JNC 7 hypertension guidelines. Author(s): Caspi O. Source: Jama : the Journal of the American Medical Association. 2003 September 10; 290(10): 1313; Author Reply 1314-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966115&dopt=Abstract
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The JNC 7 hypertension guidelines. Author(s): Sackner-Bernstein J. Source: Jama : the Journal of the American Medical Association. 2003 September 10; 290(10): 1312; Author Reply 1314-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966114&dopt=Abstract
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The JNC 7 hypertension guidelines. Author(s): Nelson MR. Source: Jama : the Journal of the American Medical Association. 2003 September 10; 290(10): 1312; Author Reply 1314-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966113&dopt=Abstract
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The JNC 7 hypertension guidelines. Author(s): Ong HT. Source: Jama : the Journal of the American Medical Association. 2003 September 10; 290(10): 1312; Author Reply 1314-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966112&dopt=Abstract
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The latest hypertension guidelines. Author(s): Hurley ML. Source: Rn. 2003 August; 66(8): 43-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13677682&dopt=Abstract
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The new hypertension guidelines from JNC 7: is the devil in the details? Author(s): Textor SC, Schwartz GL, Frye RL. Source: Mayo Clinic Proceedings. 2003 September; 78(9): 1078-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12962161&dopt=Abstract
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The nineteenth pregnancy in a patient with cor pulmonale and severe pulmonary hypertension: a management challenge. Author(s): Al-Mobeireek AF, Almutawa J, Alsatli RA. Source: Acta Obstetricia Et Gynecologica Scandinavica. 2003 July; 82(7): 676-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12790853&dopt=Abstract
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The psychosocial determinants of hypertension. Author(s): Kaplan MS, Nunes A. Source: Nutr Metab Cardiovasc Dis. 2003 February; 13(1): 52-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12772438&dopt=Abstract
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The relationship between catecholamines levels in mother and fetus, and pathogenesis of pregnancy-induced hypertension. Author(s): Zhang W, Zhao Y, Yin Y. Source: Chin Med J (Engl). 2003 July; 116(7): 1108-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890395&dopt=Abstract
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The role of magnesium sulphate in the treatment of persistent pulmonary hypertension of the newborn. Author(s): Saidy KM, Itto BA. Source: Saudi Med J. 2003 July; 24(7): 801-2. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12883626&dopt=Abstract
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Thiazides could achieve major cost savings in uncomplicated hypertension. Author(s): Mayor S. Source: Bmj (Clinical Research Ed.). 2003 September 6; 327(7414): 521. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12958099&dopt=Abstract
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Thiazides first-line treatment for hypertension. Author(s): McCormack J, Rangno R, Wright JM. Source: Can Fam Physician. 2003 July; 49: 879. English, French. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901483&dopt=Abstract
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Tibetan patients with essential hypertension caused by underlying oxidative metabolism dysfunction and depressed nitric oxide synthesis. Author(s): Li D, Wang X, Fu Z, Yu J, Da W, Peng S, Wang X. Source: Chin Med J (Engl). 2003 February; 116(2): 309-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775254&dopt=Abstract
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Transient neurologic deficits associated with carbamazepine-induced hypertension. Author(s): Marini AM, Choi JY, Labutta RJ. Source: Clinical Neuropharmacology. 2003 July-August; 26(4): 174-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12897634&dopt=Abstract
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Treatment of chronic hypertension for the prevention of stroke. Author(s): Naidech AM, Weisberg LA. Source: Southern Medical Journal. 2003 April; 96(4): 359-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12916554&dopt=Abstract
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Treatment of pulmonary arterial hypertension: a step forward. Author(s): Sharma S. Source: Chest. 2003 July; 124(1): 8-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12853493&dopt=Abstract
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Treatment of severe pulmonary hypertension with inhaled iloprost. Author(s): Leuchte HH, Baumgartner RA, Behr J. Source: Annals of Internal Medicine. 2003 August 19; 139(4): 306. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12965995&dopt=Abstract
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Trends in prevalence, awareness, treatment, and control of hypertension in the United States, 1988-2000. Author(s): Hajjar I, Kotchen TA. Source: Jama : the Journal of the American Medical Association. 2003 July 9; 290(2): 199206. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851274&dopt=Abstract
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Unclear and present danger. More vigilant hypertension treatment needed. Author(s): Diehl Y. Source: Adv Nurse Pract. 2002 October; 10(10): 73-6, 78. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12424888&dopt=Abstract
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Uncontrolled hypertension as a risk for coronary artery disease: patient characteristics and the role of physician intervention. Author(s): Hyman DJ, Pavlik VN. Source: Current Atherosclerosis Reports. 2003 March; 5(2): 131-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12573199&dopt=Abstract
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Uncontrolled hypertension due to volume overload contributes to higher left ventricular mass index in CAPD patients. Author(s): Koc M, Toprak A, Tezcan H, Bihorac A, Akoglu E, Ozener IC. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2002 September; 17(9): 1661-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12198220&dopt=Abstract
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Understanding primary pulmonary hypertension. Author(s): Berkowitz DS, Coyne NG. Source: Critical Care Nursing Quarterly. 2003 January-March; 26(1): 28-34. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12669944&dopt=Abstract
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Undertreatment of hypertension: a dozen reasons. Author(s): Gupta K, Gupta S. Source: Archives of Internal Medicine. 2002 October 28; 162(19): 2246-7; Author Reply 2247-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390071&dopt=Abstract
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Unexplained pulmonary hypertension is associated with systolic arterial hypertension in patients undergoing routine Doppler echocardiography. Author(s): Finkelhor RS, Yang SX, Bosich G, Bahler RC. Source: Chest. 2003 March; 123(3): 711-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12628867&dopt=Abstract
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Unexplained systemic hypertension after closure of ductus arteriosus. Author(s): Litwin SB. Source: Asian Cardiovascular & Thoracic Annals. 2002 December; 10(4): 379. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12538299&dopt=Abstract
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Unexplained systemic hypertension after closure of ductus arteriosus. Author(s): Aydogan U. Source: Asian Cardiovascular & Thoracic Annals. 2002 December; 10(4): 378. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12538298&dopt=Abstract
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Unrecognized internal jugular vein obstruction: cause of fatal intracranial hypertension after tracheostomy? Author(s): Schummer W, Schummer C, Niesen WD. Source: Journal of Neurosurgical Anesthesiology. 2002 October; 14(4): 313-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12357090&dopt=Abstract
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Untreated hypertension among Australian adults: the 1999-2000 Australian Diabetes, Obesity and Lifestyle Study (AusDiab). Author(s): Briganti EM, Shaw JE, Chadban SJ, Zimmet PZ, Welborn TA, McNeil JJ, Atkins RC; Australian Diabetes, Obesity and Lifestyle Study (AusDiab). Source: The Medical Journal of Australia. 2003 August 4; 179(3): 135-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885281&dopt=Abstract
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Unusual cause of intraoperative hypertension and tachycardia. Author(s): Unnikrishnan KP, Sinha PK, Neema PK. Source: Anesthesia and Analgesia. 2003 October; 97(4): 1196. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14500184&dopt=Abstract
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Update from the International Society on Hypertension in Blacks. Author(s): McCullough PA. Source: Reviews in Cardiovascular Medicine. 2002 Fall; 3(4): 192-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12650156&dopt=Abstract
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Urbanisation--the Hamlin's tune and hypertension. Author(s): Chakrabortti SCh. Source: J Indian Med Assoc. 2002 September; 100(9): 546. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12455384&dopt=Abstract
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Use of inhaled iloprost in a case of pulmonary hypertension during pediatric congenital heart surgery. Author(s): Muller M, Scholz S, Kwapisz M, Akinturk H, Thul J, Hempelmann G. Source: Anesthesiology. 2003 September; 99(3): 743-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12960561&dopt=Abstract
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Usefulness and limits of transthoracic echocardiography in the evaluation of patients with primary and chronic thromboembolic pulmonary hypertension. Author(s): Ghio S, Raineri C, Scelsi L, Recusani F, D'armini AM, Piovella F, Klersy C, Campana C, Vigano M, Tavazzi L. Source: Journal of the American Society of Echocardiography : Official Publication of the American Society of Echocardiography. 2002 November; 15(11): 1374-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12415231&dopt=Abstract
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Using the arteriolar Pressure Attenuation Index to predict ocular hypertension progression to open-angle glaucoma. Author(s): Cohen SL, Lee PP, Herndon LW, Challa P, Overbury O, Allingham RR. Source: Archives of Ophthalmology. 2003 January; 121(1): 33-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12523882&dopt=Abstract
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Uterine artery velocimetry in patients with gestational hypertension. Author(s): Frusca T, Soregaroli M, Platto C, Enterri L, Lojacono A, Valcamonico A. Source: Obstetrics and Gynecology. 2003 July; 102(1): 136-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12850619&dopt=Abstract
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Utility of ambulatory blood pressure monitoring for diagnosis of hypertension in liver allograft recipients. Author(s): Otero-Anton E, Padin E, Tome S, Gonzalez-Quintela A, Calvo C, Hermida RC, Ayala DE, Castroagudin JF, Delgado M, Varo E. Source: Transplantation Proceedings. 2003 March; 35(2): 718. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12644109&dopt=Abstract
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Utility of computed tomographic renal angiogram in the management of childhood hypertension. Author(s): Vade A, Agrawal R, Lim-Dunham J, Hartoin D. Source: Pediatric Nephrology (Berlin, Germany). 2002 September; 17(9): 741-7. Epub 2002 July 30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12215828&dopt=Abstract
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Uveal effusion and angle-closure glaucoma in primary pulmonary hypertension. Author(s): Krohn J, Bjune C. Source: American Journal of Ophthalmology. 2003 May; 135(5): 705-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12719080&dopt=Abstract
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Validation of the Microlife BP 3BTO-A oscillometric blood pressure monitoring device according to a modified British Hypertension Society protocol. Author(s): Cuckson AC, Reinders A, Shabeeh H, Shennan AH; British Hypertension Society. Source: Blood Pressure Monitoring. 2002 December; 7(6): 319-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12488652&dopt=Abstract
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Validation of the short form of the Spanish Hypertension Quality of Life Questionnaire (MINICHAL). Author(s): Badia X, Roca-Cusachs A, Dalfo A, Gascon G, Abellan J, Lahoz R, Varela C, Velasco O; MINICHAL Group. Source: Clinical Therapeutics. 2002 December; 24(12): 2137-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581551&dopt=Abstract
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Validity of the JNC VI recommendations for the management of hypertension in a general population of Japanese elderly: the Hisayama study. Author(s): Arima H, Tanizaki Y, Kiyohara Y, Tsuchihashi T, Kato I, Kubo M, Tanaka K, Ohkubo K, Nakamura H, Abe I, Fujishima M, Iida M. Source: Archives of Internal Medicine. 2003 February 10; 163(3): 361-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12578518&dopt=Abstract
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Valsartan/hydrochlorothiazide: a review of its pharmacology, therapeutic efficacy and place in the management of hypertension. Author(s): Wellington K, Faulds DM. Source: Drugs. 2002; 62(13): 1983-2005. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12215069&dopt=Abstract
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Value of rilmenidine therapy and its combination with perindopril on blood pressure and left ventricular hypertrophy in patients with essential hypertension (VERITAS). Author(s): Farsang C, Lengyel M, Borbas S, Zorandi A, Dienes BS; VERITAS Investigators. Source: Current Medical Research and Opinion. 2003; 19(3): 205-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12803735&dopt=Abstract
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Variant of pre-clinical Cushing's syndrome: hypertension and hypokalemia associated with normoreninemic normoaldosteronism. Author(s): Yamakita N, Murai T, Miyamoto K, Matsunami H, Ikeda T, Sasano H, Mune T, Yasuda K. Source: Hypertens Res. 2002 July; 25(4): 623-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12358151&dopt=Abstract
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Variation at the aldosterone synthase (CYP11B2) locus contributes to hypertension in subjects with a raised aldosterone-to-renin ratio. Author(s): Lim PO, Macdonald TM, Holloway C, Friel E, Anderson NH, Dow E, Jung RT, Davies E, Fraser R, Connell JM. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 September; 87(9): 4398-402. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12213905&dopt=Abstract
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Variceal bleeding and portal hypertension: has there been any progress in the last 12 months? Author(s): Seewald S, Mendoza G, Seitz U, Salem O, Soehendra N. Source: Endoscopy. 2003 February; 35(2): 136-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12561007&dopt=Abstract
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Vascular abnormalities in salt-sensitive hypertension. Author(s): de la Sierra A. Source: Current Hypertension Reports. 2003 April; 5(2): 93-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12642006&dopt=Abstract
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Vascular disease, hypertension, and prevention: "from endothelium to clinical events". Author(s): Hirsch AT. Source: Journal of the American College of Cardiology. 2003 July 16; 42(2): 377-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12875780&dopt=Abstract
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Vasoactive intestinal peptide as a new drug for treatment of primary pulmonary hypertension. Author(s): Petkov V, Mosgoeller W, Ziesche R, Raderer M, Stiebellehner L, Vonbank K, Funk GC, Hamilton G, Novotny C, Burian B, Block LH. Source: The Journal of Clinical Investigation. 2003 May; 111(9): 1339-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727925&dopt=Abstract
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Vasoactive modulators during and after craniotomy: relation to postoperative hypertension. Author(s): Olsen KS, Pedersen CB, Madsen JB, Ravn LI, Schifter S. Source: Journal of Neurosurgical Anesthesiology. 2002 July; 14(3): 171-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12172288&dopt=Abstract
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Vasoconstricting effect of angiotensin II in human hand veins: influence of aging, diabetes mellitus and hypertension. Author(s): Harada K, Ohmori M, Fujimura A. Source: Hypertens Res. 2002 September; 25(5): 683-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12452319&dopt=Abstract
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Venous hypertension following average arterious-venous fistula for haemodialysis. Author(s): Kojecky Z, Utikal P, Sekanina Z, Kocher M, Buriankova E. Source: Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2002 December; 146(2): 77-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12572902&dopt=Abstract
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Verification of 525 coding SNPs in 179 hypertension candidate genes in the Japanese population: identification of 159 SNPs in 93 genes. Author(s): Okuda T, Fujioka Y, Kamide K, Kawano Y, Goto Y, Yoshimasa Y, Tomoike H, Iwai N, Hanai S, Miyata T. Source: Journal of Human Genetics. 2002; 47(8): 387-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12181638&dopt=Abstract
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Visual evoked potentials in patients with Graves' ophthalmopathy complicated by ocular hypertension and suspect glaucoma or dysthyroid optic neuropathy. Author(s): Ambrosio G, Ferrara G, Vitale R, De Marco R. Source: Documenta Ophthalmologica. Advances in Ophthalmology. 2003 March; 106(2): 99-104. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678273&dopt=Abstract
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Visual field testing in patients with ocular hypertension and localized RNFL defects. Author(s): Rossetti L, Miglior S, Incarnato N, Fogangnolo P, Orzalesi N. Source: Acta Ophthalmologica Scandinavica. Supplement. 2002; 236: 27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390122&dopt=Abstract
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Visual-field loss with optic nerve drusen and ocular hypertension: a case report. Author(s): Spalding JM. Source: Optometry. 2002 January; 73(1): 24-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12363235&dopt=Abstract
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Vitamin A in the cerebrospinal fluid of patients with and without idiopathic intracranial hypertension. Author(s): Warner JE, Bernstein PS, Yemelyanov A, Alder SC, Farnsworth ST, Digre KB. Source: Annals of Neurology. 2002 November; 52(5): 647-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12402264&dopt=Abstract
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Vitamin C hypertension. Author(s): Temple RJ. Source: American Journal of Therapeutics. 2003 May-June; 10(3): 234-5; Author Reply 235. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756434&dopt=Abstract
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Vitamin E prevents extensive lipid peroxidation in patients with hypertension. Author(s): Brockes C, Buchli C, Locher R, Koch J, Vetter W. Source: British Journal of Biomedical Science. 2003; 60(1): 5-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12680623&dopt=Abstract
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What defines an adolescent as having hypertension? Author(s): Materson BJ. Source: Journal of Hypertension. 2003 January; 21(1): 13-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12544425&dopt=Abstract
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What is the meaning of LIFE? Implications of the Losartan Intervention for Endpoint reduction in hypertension trial for heart failure physicians. Author(s): Massie BM. Source: Journal of Cardiac Failure. 2002 August; 8(4): 197-201. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12397565&dopt=Abstract
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When can the practicing physician suspect white coat hypertension? Statement from the Working Group on Blood Pressure Monitoring of the European Society of Hypertension. Author(s): Verdecchia P, O'Brien E, Pickering T, Staessen JA, Parati G, Myers M, Palatini P; European Society of Hypertension Working Group on Blood Pressure Monitoring. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2003 January; 16(1): 87-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12517690&dopt=Abstract
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White coat effect and white coat hypertension in pediatric patients. Author(s): Matsuoka S, Kawamura K, Honda M, Awazu M. Source: Pediatric Nephrology (Berlin, Germany). 2002 November; 17(11): 950-3. Epub 2002 October 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12432440&dopt=Abstract
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White coat hypertension and nursing care. Author(s): Alves LM, Nogueira MS, Veiga EV, de Godoy S, Carnio EC. Source: Can J Cardiovasc Nurs. 2003; 13(3): 29-34. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14508916&dopt=Abstract
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White coat hypertension in treated hypertensives: a three year follow-up study. Author(s): MacDonald MB, Laing GP, Wilson MP, Wilson TW. Source: Can J Cardiovasc Nurs. 2003; 13(2): 24-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802835&dopt=Abstract
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White coat hypertension in Zimbabwean African women. Author(s): Bhagat K. Source: East Afr Med J. 2000 August; 77(8): 452-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12862073&dopt=Abstract
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White coat hypertension: understanding the concept and examining the significance. Author(s): Tsai PS. Source: Journal of Clinical Nursing. 2002 November; 11(6): 715-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12427175&dopt=Abstract
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White coat hypertension'--should it be treated or not? Author(s): Pickering T. Source: Cleve Clin J Med. 2002 August; 69(8): 584-5. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12184466&dopt=Abstract
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White-coat effect in normotension and hypertension. Author(s): Zakopoulos NA, Kotsis VT, Pitiriga VCh, Toumanidis ST, Lekakis JP, Nanas SN, Vemmos KN, Stamatelopoulos SF, Moulopoulos SD. Source: Blood Pressure Monitoring. 2002 October; 7(5): 271-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12409886&dopt=Abstract
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White-coat hypertension and normotension in the League of Hypertension of the Hospital das Clinicas, FMUSP: prevalence, clinical and demographic characteristics. Author(s): Segre CA, Ueno RK, Warde KR, Accorsi TA, Miname MH, Chi CK, Pierin AM, Mion Junior D. Source: Arquivos Brasileiros De Cardiologia. 2003 February; 80(2): 117-26. Epub 2003 February 25. English, Portuguese. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640506&dopt=Abstract
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Why beta-blockers are not cardioprotective in elderly patients with hypertension. Author(s): Grossman E, Messerli FH. Source: Current Cardiology Reports. 2002 November; 4(6): 468-73. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12379165&dopt=Abstract
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Why not prescribe the best drugs for hypertension now? Author(s): Wong SY, McInnes GT, MacDonald TM. Source: Journal of Human Hypertension. 2003 July; 17(7): 505-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12821958&dopt=Abstract
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Why we can't translate clinical trials into clinical practice in hypertension. Author(s): Resnick LM. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2003 May; 16(5 Pt 1): 421-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745206&dopt=Abstract
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CHAPTER 2. NUTRITION AND HYPERTENSION Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and hypertension.
Finding Nutrition Studies on Hypertension The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “hypertension” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7
Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
176 Hypertension
The following is a typical result when searching for recently indexed consumer information on hypertension: •
Authorized health claims. Source: FDA-consumer (USA). (Nov-December 1998). volume 32(6) page 19-21. calcium osteodystrophy sodium hypertension diet fats neoplasms saturated fats cholesterol heart diseases risk dietary fibres solubility cereals grain fruits vegetables folic acid dental caries sugar alcohols 0362-1332
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Diet for keeping blood pressure down. Source: Tufts-University-diet-and-nutrition-letter (USA). (July 1996). volume 14(5) page 6. diet blood pressure hypertension weight reduction alcoholic beverages physical activity potassium sodium chloride common salt 0747-4105
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Effects of individual fatty acids on chronic diseases. Author(s): Penn State University. Source: Jonnalagadda, S.S. Mustad, V.A. Yu, S. Etherton, T.D. Kris Etherton, P.M. Nutrition-today (USA). (June 1996). volume 31(3) page 90-106. fatty acids food consumption diet fats nutrients nutrient intake heart diseases hypertension neoplasms diabetes thrombosis chronic course immune response saturated fatty acids unsaturated fatty acids risk 0029-666X
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For men only: a primer on your unique nutrition concerns. Source: Helm, J. Environmental-nutrition (USA). (June 1997). volume 20(6) page 1, 4-5. men nutritional requirements diet foods neoplasms prostate hypertension adipose tissues overweight osteodystrophy disease control iron folic acid pyridoxine proteins zinc 0893-4452
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Genetic variation and nutrition. 2. Genetic variation, nutrition, and chronic diseases. Author(s): Center for Genetics Nutrition and Health, Washington, DC. Source: Simopoulos, A.P. Nutrition-today (USA). (October 1995). volume 30(5) page 194206. genotype environment interaction overweight carcinomas autoimmune diseases chronic course genetic variation pathogenesis risk hypertension diet families genetic disorders disease control recommended dietary allowances diabetes osteodystrophy 0029-666X
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Good news about what to eat to take control of your blood pressure. Source: Walsh, J. Environmental-nutrition (USA). (December 1998). volume 21(12) page 1, 6. diet food intake common salt hypertension clinical trials human nutrition 0893-4452
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One nation, under pressure. Source: Liebman, B. Nutrition-action-health-letter (USA). (Jul-August 1995). volume 22(6) page 1, 4-9. blood pressure hypertension risk therapeutic diets sodium weight reduction physical activity 0885-7792
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Reexamining cholesterol and sodium recommendations. Source: Callaway, W. Nutrition-today (USA). (October 1994). volume 29(5) page 32-36. cholesterol sodium recommended dietary allowances diet blood lipids cardiovascular diseases hypertension case studies 0029-666X
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Scouting for sodium: and other nutrients important to blood pressure. Source: Kurtzweil, P. FDA-consumer (USA). (September 1994). volume 28(7) page 18-22. usa sodium blood pressure hypertension therapeutic diets nutrition labelling 0362-1332
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The fetal origins of adult disease. Author(s): University of Southampton, Southampton, England.
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Source: Barker, D.J.P. Nutrition-today (USA). (June 1996). volume 31(3) page 108-114. embryonic development mothers human nutrition malnutrition overweight adults heart diseases birth weight diabetes hypertension cardiovascular diseases muscles growth infants body measurements placenta multiple births 0029-666X •
To shake or not to shake: EN takes another look at salt. Source: Ternus, M. Environmental-nutrition (USA). (September 1996). volume 19(9) page 1, 4. sodium chloride common salt nutritive value osteodystrophy flavour enhancers hypertension risk nutrient excesses meal patterns dietary guidelines age recommended dietary allowances calcium absorption nutrient intake men women 08934452
Additional consumer oriented references include: •
Array of drugs tames hypertension. Lessening the pressure. Source: Kurtzweil, P FDA-Consum. 1999 Jul-August; 33(4): 18-23 0362-1332
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Calcium and hypertension: does a relationship exist. Source: Thomson, A.B.R. Nutr-Today. Baltimore, Md. : Williams & Wilkins. July/August 1989. volume 24 (4) page 21-26. 0029-666X
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Diabetes and hypertension. Source: Beach, R.S. Diabetes-Forecast. Alexandria, Va. : American Diabetes Association. April 1989. volume 42 (4) page 54-60. charts. 0095-8301
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I am undergoing treatment for hypertension and have been taking 200 mg of vitamin E daily for the past few years. I read that even lower doses might raise my risk of having a hemorrhagic stroke. Is this true? Source: Goldfinger, S E Harv-Health-Lett. 1999 January; 24(3): 3 1052-1577
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I have mild hypertension and my doctor recommended I eat bananas and drink orange juice. Why? Source: Anonymous Johns-Hopkins-Med-Lett-Health-After-50. 1999 August; 11(6): 8 1042-1882
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I recently read that potassium supplements can reduce blood pressure. What is your opinion? I have borderline hypertension, which I'm trying to control with diet and exercise. Source: Robb Nicholson, C Harv-Womens-Health-Watch. 1999 January; 6(5): 8 1070910X
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Magnesium and other nutrient deficiencies as possible causes of hypertension and low birthweight. Source: Wynn, A Wynn, M Nutr-Health. 1988; 6(2): 69-88 0260-1060
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Recommendations updated for hypertension. Source: Anonymous Harv-Health-Lett. 1998 January; 23(3): 6-7 1052-1577
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Reduced cardiovascular morbidity and mortality in hypertensive diabetic patients on first-line therapy with an ACE inhibitor compared with a diuretic/beta-blocker-based treatment regimen: a subanalysis of the Captopril Prevention Project. Author(s): Department of Medicine, University of Kuopio, Kuopio, Finland.
[email protected] Source: Niskanen, L Hedner, T Hansson, L Lanke, J Niklason, A Diabetes-Care. 2001 December; 24(12): 2091-6 0149-5992
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The brown eyes are from Dad, the hypertension from Mom. Source: Warshaw, H. Environ-Nutr. New York, N.Y. : Environmental Nutrition, Inc. October 1990. volume 13 (10) page 1, 6. 0893-4452
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Urinary transforming growth factor-beta excretion in patients with hypertension, type 2 diabetes, and elevated albumin excretion rate: effects of angiotensin receptor blockade and sodium restriction. Author(s): University of Melbourne, Department of Medicine at Austin, Victoria, Australia. Source: Houlihan, C A Akdeniz, A Tsalamandris, C Cooper, M E Jerums, G Gilbert, R E Diabetes-Care. 2002 June; 25(6): 1072-7 0149-5992
The following information is typical of that found when using the “Full IBIDS Database” to search for “hypertension” (or a synonym): •
Immunoreactivity and inhibition of angiotensin I converting enzyme and lactococcal oligopeptidase by peptides from cheese. Author(s): Agricultural Univ. of Norway, As. Dept. of Food Science Polish Academy of Sciences, Poznan (Poland). Inst. of Food Science Source: Stepaniak, L. SorhAugust, T. Jedrychowski, L. Wroblewska, B. Italian-Journalof-Food-Science (Italy). (2001). volume 13(4) page 373-381. cheese hypertension inhibition immunological techniques analytical methods lactococcus lactis enzymes enzymatic analysis hplc peptides 1120-1770
Additional physician-oriented references include: •
A comparative clinical study of latanoprost and isopropyl unoprostone in Japanese patients with primary open-angle glaucoma and ocular hypertension. Author(s): Department of Opthalmology and Visual Science, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan. Source: Tsukamoto, H Mishima, H K Kitazawa, Y Araie, M Abe, H Negi, A J-Glaucoma. 2002 December; 11(6): 497-501 1057-0829
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A nested case-control study on the high-normal blood pressure as a risk factor of hypertension in Korean middle-aged men. Author(s): Department of Preventive Medicine, Cheju National University College of Medicine, Cheju, Korea.
[email protected] Source: Bae, J M Ahn, Y O J-Korean-Med-Sci. 2002 June; 17(3): 328-36 1011-8934
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Activation of hypothalamic angiotensin receptors produces pressor responses via cholinergic inputs to the rostral ventrolateral medulla in normotensive and hypertensive rats. Source:
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Altered vascular function in fetal programming of hypertension. Author(s): Research Center, Hopital Sainte-Justine, Department of Pediatrics and Pharmacology, Universite de Montreal, Montreal, Canada. Source: Lamireau, D Nuyt, A M Hou, X Bernier, S Beauchamp, M Gobeil, F Jr Lahaie, I Varma, D R Chemtob, S Stroke. 2002 December; 33(12): 2992-8 1524-4628
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Antihypertensive effect of sesamin. IV. Inhibition of vascular superoxide production by sesamin. Author(s): Department of Pharmacology, Osaka University of Pharmaceutical Sciences, Takatsuki, Japan.
Nutrition 179
Source: Nakano, D Itoh, C Takaoka, M Kiso, Y Tanaka, T Matsumura, Y Biol-PharmBull. 2002 September; 25(9): 1247-9 0918-6158 •
Antihypertensive effects of valsartan/hydrochlorothiazide combination in essential hypertension. Source: Schmidt, A Adam, S A Kolloch, R Weidinger, G Handrock, R Blood-Press. 2001; 10(4): 230-7 0803-7051
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Blood pressure response to antihypertensive agents related to baseline blood pressure. Author(s): Cardiovascular Unit, Department of Medicine, Bangkok Metropolitan Administration Medical College and Vajira Hospital, Bangkok 10300, Thailand. Source: Sermswan, A Uboldejpracharak, Y Suthichaiyakul, T Sukontasarn, A Buranakitcharoen, P J-Med-Assoc-Thai. 2002 October; 85(10): 1113-20 0125-2208
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Cardiovascular effects of the essential oil of Mentha x villosa in DOCA-salthypertensive rats. Author(s): Departamento de Fisiologia e Farmacologia, Centro de Ciencias Biologicas, Universidade Federal de Pernambuco, Recife-PE, Brasil.
[email protected] Source: Lahlou, S Carneiro Leao, R F Leal Cardoso, J H Phytomedicine. 2002 December; 9(8): 715-20 0944-7113
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Combination therapy with an angiotensin-converting enzyme (ACE) inhibitor and a calcium antagonist: beyond the renoprotective effects of ACE inhibitor monotherapy in a spontaneous hypertensive rat with renal ablation. Author(s): Department of Internal Medicine and Rehabilitation Science, Tohoku University Graduate School of Medicine, Sendai, Japan.
[email protected] Source: Kanazawa, M Kohzuki, M Yoshida, K Kurosawa, H Minami, N Saito, T Yasujima, M Abe, K Hypertens-Res. 2002 May; 25(3): 447-53 0916-9636
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Combination treatment with a calcium channel blocker and an angiotensin blocker in a rat systolic heart failure model with hypertension. Author(s): Department of Pharmacology, Osaka City University Medical School, Japan. Source: Namba, M Kim, S Zhan, Y Nakao, T Iwao, H Hypertens-Res. 2002 May; 25(3): 461-6 0916-9636
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Comparison of latanoprost, brimonidine and a fixed combination of timolol and dorzolamide on circadian intraocular pressure in patients with primary open-angle glaucoma and ocular hypertension. Author(s): University Eye Clinic, San Paolo Hospital, Milan. Source: Orzalesi, N Rossetti, I Bottoli, A Invernizzi, T Fumagalli, E Fogagnolo, P ActaOphthalmol-Scand-Suppl. 2002; 236: 55 1395-3931
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Darusentan: an effective endothelinA receptor antagonist for treatment of hypertension. Source:
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Decreased 4-aminopyridine sensitive K+ currents in endothelial cells from hypertensive rats. Author(s): Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Source: Sadanaga, T Ohya, Y Ohtsubo, T Goto, K Fujii, K Abe, I Hypertens-Res. 2002 July; 25(4): 589-96 0916-9636
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Differential effects of a long-acting angiotensin converting enzyme inhibitor (temocapril) and a long-acting calcium antagonist (amlodipine) on ventricular ectopic beats in older hypertensive patients. Author(s): Department of Internal Medicine, Nishiarita Kyoritsu Hospital, Saga, Japan.
[email protected] Source: Eguchi, K Kario, K Shimada, K Hypertens-Res. 2002 May; 25(3): 329-33 09169636
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Effect of acute portal hypertension on gut mucosa. Author(s): Second Department of Surgery, Kinki University School of Medicine, 377-2 Ohno-Higashi, Osaka, Sayama, Osaka 589-8511, Japan. Source: Hashimoto, N Ohyanagi, H Hepatogastroenterology. 2002 Nov-December; 49(48): 1567-70 0172-6390
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Effect of long-term intake of milk products on blood pressure in hypertensive rats. Author(s): Institute of Biomedicine, Pharmacology, Biomedicum Helsinki, University of Helsinki, Finland.
[email protected] Source: Sipola, M Finckenberg, P Korpela, R Vapaatalo, H Nurminen, M L J-Dairy-Res. 2002 February; 69(1): 103-11 0022-0299
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Effect of renin-angiotensin system activation by dietary sodium restriction and upright position on plasma leptin concentration in patients with essential hypertension. Author(s): Department of Nephrology, Endocrinology and Metabolic Diseases, Silesian Medical University, Katowice, Poland. Source: Adamczak, M Kokot, F Chudek, J Wiecek, A Med-Sci-Monit. 2002 July; 8(7): CR473-7 1234-1010
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Effects of angiotensin converting enzyme inhibitor and calcium antagonist on endothelial function in patients with essential hypertension. Author(s): Department of Internal Medicine, Soonchunhyang University, College of Medicine, Seoul, Korea.
[email protected] Source: On, Y K Kim, C H Oh, B H Lee, M M Park, Y B Hypertens-Res. 2002 May; 25(3): 365-71 0916-9636
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Effects of atorvastatin on aortic pulse wave velocity in patients with hypertension and hypercholesterolaemia: a preliminary study. Author(s): Department of Internal Medicine, Broussaia Hospital, Paris, France. Source: Raison, J Rudnichi, A Safar, M E J-Hum-Hypertens. 2002 October; 16(10): 705-10 0950-9240
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Effects of caloric restriction on development of the proximal growth plate and metaphysis of the caput femoris in spontaneously hypertensive rats: microscopic and computer-assisted image analyses. Author(s): Department of Respiratory and Digestive Medicine, Nagasaki University School of Medicine, Nagasaki City 852-8102, Japan.
[email protected] Source: Kawahara, T Shimokawa, I Tomita, M Hirano, T Shindo, H Microsc-Res-Tech. 2002 November 15; 59(4): 306-12 1059-910X
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Effects of four antihypertensive monotherapies on cardiac mass and function in hypertensive patients with left ventricular hypertrophy: randomized prospective study. Author(s): Department of Internal Medicine, Split University Hospital and School of Medicine, Split, Croatia.
[email protected] Source: Rakic, D Rumboldt, Z Bagatin, J Polic, S Croat-Med-J. 2002 December; 43(6): 6729 0353-9504
Nutrition 181
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Effects of Ginkgo biloba extract (EGb 761) on cerebral thrombosis and blood pressure in stroke-prone spontaneously hypertensive rats. Author(s): Laboratory of Physiology, Faculty of Nutrition, Kobe Gakuin University, Kobe, Japan.
[email protected] Source: Sasaki, Y Noguchi, T Yamamoto, E Giddings, J C Ikeda, K Yamori, Y Yamamoto, J Clin-Exp-Pharmacol-Physiol. 2002 November; 29(11): 963-7 0305-1870
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Effects of L-carnosine on renal sympathetic nerve activity and DOCA-salt hypertension in rats. Author(s): Niigata University School of Medicine, Asahimachidoori, Japan.
[email protected] Source: Niijima, A Okui, T Matsumura, Y Yamano, T Tsuruoka, N Kiso, Y Nagai, K Auton-Neurosci. 2002 May 31; 97(2): 99-102 1566-0702
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Effects of policosanol on older patients with hypertension and type II hypercholesterolaemia. Author(s): Surgical Medical Research Center, Havana City, Cuba. Source: Castano, G Mas, R Fernandez, J C Fernandez, L Illnait, J Lopez, E Drugs-R-D. 2002; 3(3): 159-72 1174-5886
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Effects of stress and behavioral interventions in hypertension: the rise and fall of omapatrilat. Author(s): Integrative and Behavioral Cardiovascular Health Program, Zena and Michael Wiener Cardiovascular Institute, Mt. Sinai School of Medicine, New York, NY 10029, USA. Source: Pickering, T G J-Clin-Hypertens-(Greenwich). 2002 Sep-October; 4(5): 371-3 1524-6175
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Efficacy and safety of a therapeutic interchange from high-dose calcium channel blockers to a fixed-dose combination of amlodipine/benazepril in patients with moderate-to-severe hypertension. Source: Caro, J J Lee, K Curr-Hypertens-Repage 2002 December; 4(6): 417-8 1522-6417
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Emerging medical therapies for pulmonary arterial hypertension. Author(s): Institute of Cardiology, University of Bologna, Italy. Source: Galie, N Manes, A Branzi, A Prog-Cardiovasc-Dis. 2002 Nov-December; 45(3): 213-24 0033-0620
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Endothelium-dependent vasorelaxation induced by L-carnitine in isolated aorta from normotensive and hypertensive rats. Author(s): Department of Pharmacology, Faculty of Pharmacy, University of Seville, C/ Profesor Garcia Gonzalez s/n, 41012-Seville, Spain.
[email protected] Source: Herrera, M D Bueno, R De Sotomayor, M A Perez Guerrero, C Vazquez, C M Marhuenda, E J-Pharm-Pharmacol. 2002 October; 54(10): 1423-7 0022-3573
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Ethnopharmacobotany in Tuscany: plants used as antihypertensives. Author(s): Dipartimento di Agronomia e Gestione dell'Agroecosistema via S. Michele degli Scalzi, 2-56100, Pisa, Italy. Source: Uncini Manganelli, R E Chericoni, S Baragatti, B Fitoterapia. 2000 August; 71 Suppl 1: S95-100 0367-326X
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Fluvastatin remodels resistance arteries in genetically hypertensive rats, even in the absence of any effect on blood pressure. Author(s): Department of Pharmacology and Toxicology, School of Medical Sciences, University of Otago, Dunedin, New Zealand.
[email protected]
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Source: Ledingham, J M Laverty, R Clin-Exp-Pharmacol-Physiol. 2002 October; 29(10): 931-4 0305-1870 •
Hemostasis imbalance in experimental hypertension. Author(s): INSERM U479, Faculte Xavier Bichat, Paris, France. Source: Corseaux, D Ollivier, V Fontaine, V Huisse, M G Philippe, M LoueDecember, L Vranckx, R Ravanat, C Lanza, F Angles Cano, E Guillin, M C Michel, J B Mol-Med. 2002 April; 8(4): 169-78 1076-1551
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High salt intake inhibits nitric oxide synthase expression and aggravates hypertension in rats with chronic renal failure. Author(s): Department of Medicine, Keck School of Medicine University of Southern California, Los Angeles, USA.
[email protected] Source: Campese, V M Mozayeni, P Ye, S Gumbard, M J-Nephrol. 2002 Jul-August; 15(4): 407-13 1120-3625
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HMG-CoA reductase inhibitor has protective effects against stroke events in strokeprone spontaneously hypertensive rats. Author(s): Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
[email protected] Source: Kawashima, S Yamashita, T Miwa, Y Ozaki, M Namiki, M Hirase, T Inoue, N Hirata, K Yokoyama, M Stroke. 2003 January; 34(1): 157-63 1524-4628
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Hypertension and insulin disorders. Author(s): Division of Internal Medicine, Ajina Tsuchiya Hospital, 4-51-1 Ajina Hatsukaichi, Japan.
[email protected] Source: Imazu, M Curr-Hypertens-Repage 2002 December; 4(6): 477-82 1522-6417
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Hypertensive cardiovascular disease: risk reduction by dietary calcium and dairy foods. Source: McCarron, D.A. Reusser, M.E. Sciences-des-Aliments (France). (2002). volume 22(4) page 415-421. Numero special: Dairy Products, Nutrition and Health. P11. calcium diet milk products hypertension human nutrition health 0240-8813
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Initial treatment of hypertension. Author(s): Weill Medical College of Cornell University and the Lang Research Center, New York Hospital Medical Center of Queens, New York, USA. Source: August, P N-Engl-J-Med. 2003 February 13; 348(7): 610-7 1533-4406
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Insights into Dahl salt-sensitive hypertension revealed by temporal patterns of renal medullary gene expression. Author(s): Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
[email protected] Source: Liang, M Yuan, B Rute, E Greene, A S Olivier, M Cowley, A W Jr PhysiolGenomics. 2003 February 6; 12(3): 229-37 1531-2267
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Is lead exposure the principal cause of essential hypertension? Author(s): Nephrology Division, The Burns and Allen Research Institute, Cedars-Sinai Medical Center, Los Angeles 90048, USA.
[email protected] Source: Gonick, H C Behari, J R Med-Hypotheses. 2002 September; 59(3): 239-46 03069877
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Isradipine treatment of hypertension in children: a single-center experience. Author(s): Division of Pediatric Nephrology, Montefiore Medical Center, Bronx, NY 10467, USA.
[email protected] Source: Flynn, J T Warnick, S J Pediatr-Nephrol. 2002 September; 17(9): 748-53 0931-041X
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Mecamylamine (Inversine): an old antihypertensive with new research directions. Author(s): Center for Aging and Brain Repair, Department of Neurosurgery, University of South Florida College of Medicine, Tampa 33613, USA.
[email protected] Source: Shytle, R D Penny, E Silver, A A Goldman, J Sanberg, P R J-Hum-Hypertens. 2002 July; 16(7): 453-7 0950-9240
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Molecular and cellular basis of pulmonary vascular remodeling in pulmonary hypertension. Author(s): Respiratory Medicine Unit, Department of Medicine, Addenbrooke's Hospital, University of Cambridge School of Clinical Medicine, Cambridge, UK. Source: Jeffery, T K Morrell, N W Prog-Cardiovasc-Dis. 2002 Nov-December; 45(3): 173202 0033-0620
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Non pharmacologic therapy and lifestyle factors in hypertension. Author(s): Department of Medicine, University of Western Australia, Royal Perth Hospital, Australia. Source: Beilin, L J Burke, V Cox, K L Hodgson, J M Mori, T A Puddey, I B Blood-Press. 2001; 10(5-6): 352-65 0803-7051
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Nutritional supplementation with Chlorella pyrenoidosa for mild to moderate hypertension. Author(s): Department of Anatomy and Internal Medicine, Virginia Commonwealth University, Medical College of Virginia, Richmond, VA 23298-0709, USA.
[email protected] Source: Merchant, R E Andre, C A Sica, D A J-Med-Food. 2002 Fall; 5(3): 141-52 1096620X
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Participation of renal and circulating endothelin in salt-sensitive essential hypertension. Author(s): Department of Medicine, College of Human Medicine, Michigan State University, Medical Education and Research Center of Grand Rapids, 49503, USA.
[email protected] Source: Elijovich, F Laffer, C L J-Hum-Hypertens. 2002 July; 16(7): 459-67 0950-9240
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Pulmonary hypertension associated with connective tissue disease. Author(s): Pulmonary Hypertension Center, University of Colorado Health Sciences Center, Denver, CO, USA. Source: Fagan, K A Badesch, D B Prog-Cardiovasc-Dis. 2002 Nov-December; 45(3): 22534 0033-0620
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Pulmonary hypertension in systemic sclerosis: bete noire no more? Source: Varga, J Curr-Opin-Rheumatol. 2002 November; 14(6): 666-70 1040-8711
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Recent developments in the treatment of obesity-related hypertension. Author(s): Franz Volhard Clinic - HELIOS-Klinikum Berlin Buch, Charite, Medical Faculty of the Humboldt University Berlin, Max Delbruck Center for Molecular Medicine, Germany. Source: Pischon, T Sharma, A M Curr-Opin-Nephrol-Hypertens. 2002 September; 11(5): 497-502 1062-4821
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Responsiveness, affinity constants and beta-adrenoceptor reserves for isoprenaline on aortae from normo-, pre- and hypertensive rats. Author(s): Cardiovascular Pharmacology Group, Faculty of Medicine and Health Science, The University of Auckland, New Zealand. Source: Chen, Y Y Doggrell, S A J-Pharm-Pharmacol. 2002 April; 54(4): 515-22 0022-3573
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Role of bacterial cell wall proteinase in anti hypertension. Author(s): (Chr. Hansen A/S, Hoersholm (Danemark)) Source: Flambard, B. Sciences-des-Aliments (France). (2002). volume 22(1-2) page 209222. P11. lactic acid bacteria cell walls proteases medicinal properties hypertension 02408813
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Role of blood pressure monitoring in non-pharmacological management of hypertension. Author(s): Division of Hypertension and Nephrology, National Cardiovascular Centre, Suita, Osaka, Japan. Source: Kawano, Y Blood-Press-Monit. 2002 February; 7(1): 51-4 1359-5237
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Subjects with essential hypertension are more sensitive to the inhibition of 11 betaHSD by liquorice. Source: Sigurjonsdottir, H A Manhem, K Axelson, M Wallerstedt, S J-Hum-Hypertens. 2003 February; 17(2): 125-31 0950-9240
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The effect of amlodipine on exercise-induced pulmonary hypertension and right heart function in patients with chronic obstructive pulmonary disease. Author(s): Klinik Wehrawald, BfA Schwarzenbacher Strasse 3 79682 Todtmoos, Germany.
[email protected] Source: Franz, I W Van Der Meyden, J Schaupp, S Tonnesmann, U Z-Kardiol. 2002 October; 91(10): 833-9 0300-5860
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The effect of the combination of Mediterranean diet and leisure time physical activity on the risk of developing acute coronary syndromes, in hypertensive subjects. Author(s): Cardiology Department, School of Medicine, University of Athens, Greece. Source: Pitsavos, C Panagiotakos, D B Chrysohoou, C Kokkinos, P F Skoumas, J Papaioannou, I Stefanadis, C Toutouzas, P J-Hum-Hypertens. 2002 July; 16(7): 517-24 0950-9240
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Use of atorvastatin in hyperlipidemic hypertensive renal transplant recipients. Author(s): Department of Molecular Medicine, Karolinska Institutet, L3 Karolinska Hospital, 171 76 Stockholm, Sweden.
[email protected] Source: KrMarch, R T Ferraris, J R Ramirez, J A Sorroche, P Legal, S Cayssials, A PediatrNephrol. 2002 July; 17(7): 540-3 0931-041X
Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
The following is a specific Web list relating to hypertension; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
Vitamins Vitamin B6 Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin C Source: Healthnotes, Inc. www.healthnotes.com Vitamin C Source: Prima Communications, Inc.www.personalhealthzone.com
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Minerals ACE Inhibitors (Angiotensin-Converting Enzyme Inhibitors) Source: Prima Communications, Inc.www.personalhealthzone.com
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Angiotensin-Converting Enzyme (ACE) Inhibitors Source: Healthnotes, Inc. www.healthnotes.com Angiotensin-Converting Enzyme (ACE) Inhibitors Source: Integrative Medicine Communications; www.drkoop.com Calcium Source: Healthnotes, Inc. www.healthnotes.com Calcium Source: Prima Communications, Inc.www.personalhealthzone.com Calcium-Channel Blockers Source: Healthnotes, Inc. www.healthnotes.com HMG-CoA Reductase Inhibitors (Statins) Source: Integrative Medicine Communications; www.drkoop.com L-Carnitine Source: Healthnotes, Inc. www.healthnotes.com Magnesium Source: Healthnotes, Inc. www.healthnotes.com Magnesium Source: Integrative Medicine Communications; www.drkoop.com Magnesium Source: Prima Communications, Inc.www.personalhealthzone.com Potassium Source: Healthnotes, Inc. www.healthnotes.com Potassium Source: Integrative Medicine Communications; www.drkoop.com Potassium Source: Prima Communications, Inc.www.personalhealthzone.com Potassium Chloride Source: Healthnotes, Inc. www.healthnotes.com Spironolactone Source: Healthnotes, Inc. www.healthnotes.com Zinc Source: Healthnotes, Inc. www.healthnotes.com Zinc Source: Integrative Medicine Communications; www.drkoop.com
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Food and Diet Artichoke Source: Healthnotes, Inc. www.healthnotes.com Atkins Diet Source: Healthnotes, Inc. www.healthnotes.com Avocado Source: Healthnotes, Inc. www.healthnotes.com Beets Source: Healthnotes, Inc. www.healthnotes.com Chocolate Source: Healthnotes, Inc. www.healthnotes.com Coffee Source: Healthnotes, Inc. www.healthnotes.com Diabetes Source: Healthnotes, Inc. www.healthnotes.com Garlic Alternative names: Allium sativum Source: Healthnotes, Inc. www.healthnotes.com Garlic Source: Prima Communications, Inc.www.personalhealthzone.com Garlic Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,786,00.html Hypertension Source: Healthnotes, Inc. www.healthnotes.com Jerusalem Artichoke Source: Healthnotes, Inc. www.healthnotes.com Kohlrabi Source: Healthnotes, Inc. www.healthnotes.com Low Back Pain Source: Healthnotes, Inc. www.healthnotes.com Low-Fat Diet Source: Healthnotes, Inc. www.healthnotes.com Low-Salt Diet Source: Healthnotes, Inc. www.healthnotes.com
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Natural Sweeteners Source: Healthnotes, Inc. www.healthnotes.com Nutritional Yeast Source: Integrative Medicine Communications; www.drkoop.com Nutritional Yeast Alternative names: Brewer's Yeast Source: Integrative Medicine Communications; www.drkoop.com Omega-3 Fatty Acids Source: Integrative Medicine Communications; www.drkoop.com Omega-3 fatty acids Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,992,00.html Parsnips Source: Healthnotes, Inc. www.healthnotes.com Porcini Mushrooms Source: Healthnotes, Inc. www.healthnotes.com Radishes Source: Healthnotes, Inc. www.healthnotes.com Rutabagas Source: Healthnotes, Inc. www.healthnotes.com Salmon Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/foods_view/0,1523,102,00.html Shiitake Mushrooms Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/foods_view/0,1523,308,00.html Special Diets Index Source: Healthnotes, Inc. www.healthnotes.com Tea Source: Healthnotes, Inc. www.healthnotes.com The Dean Ornish Diet Source: Healthnotes, Inc. www.healthnotes.com Tyramine-Free Diet Source: Healthnotes, Inc. www.healthnotes.com
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Vegetarian Diet Source: Healthnotes, Inc. www.healthnotes.com Weight Loss and Obesity Source: Healthnotes, Inc. www.healthnotes.com Winter Squash Source: Healthnotes, Inc. www.healthnotes.com Yams Source: Healthnotes, Inc. www.healthnotes.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND HYPERTENSION Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to hypertension. At the conclusion of this chapter, we will provide additional sources.
The Combined Health Information Database The Combined Health Information Database (CHID) is a bibliographic database produced by health-related agencies of the U.S. federal government (mostly from the National Institutes of Health) that can offer concise information for a targeted search. The CHID database is updated four times a year at the end of January, April, July, and October. Check the titles, summaries, and availability of CAM-related information by using the “Simple Search” option at the following Web site: http://chid.nih.gov/simple/simple.html. In the drop box at the top, select “Complementary and Alternative Medicine.” Then type “hypertension” (or synonyms) in the second search box. We recommend that you select 100 “documents per page” and to check the “whole records” options. The following was extracted using this technique: •
Using the Body To Heal the Body: Exercise and Disease Intervention Source: Alternative and Complementary Therapies. 4(3): 169-172. June 1998. Summary: This journal article discusses the multiple health benefits of exercise, highlighting the work in this area by Dr. L. Goldberg and D. L. Elliot at the Human Performance Laboratory, Division of Health Promotion and Sports Medicine, Oregon Health Sciences University in Portland. Drs. Goldberg and Elliot have focused their work on the effects of exercise in hypertension, neuromuscular diseases, certain metabolic conditions, and obesity. Clinicians at the Human Performance Laboratory offer patients a choice of testing options, and develop individualized exercise plans specifying exercise mode, intensity, duration, frequency, and progression. They also help patients develop strategies to overcome potential barriers to plan compliance. Exercise, along with diet, stress reduction, and social support, also is an integral component of the Opening Your Heart Program developed by Dr. D. Ornish at the Preventive Medicine Research Center in Sausalito, California. Dr. Ornish emphasizes
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that exercise does not have to be vigorous to be beneficial, noting that consistency is more important than intensity. In addition to its benefits in heart disease, recent research suggests a role for exercise in reducing cancer risk and improving function in older age. The article includes a list of recommended readings and 14 references. •
Herbal Medicines: Poison or Potions? Source: Journal of Laboratory and Clinical Medicine. 139(6): 343-8. June 2002. Summary: This journal article provides a wide variety of information on herbal medicines, including the reasons for their use, safety issues, beneficial effects, adverse effects, and the role that physicians can play in helping patients make informed treatment decisions. The article gives examples of adverse effects from specific herbs, including: Herbal Ecstasy and Parkinson's syndrome; Chinese medications with undeclared prescription drugs; Indian herbal medications with lead contamination; valerian withdrawal syndrome; adverse reactions of St. John's wort; mu tong and nephropathy; saw palmetto and liver disease; dong quai and hypertension; and kombucha mushroom and coagulation disorders. 1 table. 38 references. 6 pages.
National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to hypertension and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “hypertension” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to hypertension: •
A preliminary fast may potentiate response to a subsequent low-salt, low-fat vegan diet in the management of hypertension - fasting as a strategy for breaking metabolic vicious cycles. Author(s): McCarty MF. Source: Medical Hypotheses. 2003 May; 60(5): 624-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12710893&dopt=Abstract
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Acupuncture in hypertension. Author(s): Townsend RR. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2002 May-June; 4(3): 229. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12045377&dopt=Abstract
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Acute effect of tetrandrine pulmonary targeting microspheres on hypoxic pulmonary hypertension in rats. Author(s): Cheng D, Chen W, Mo X. Source: Chin Med J (Engl). 2002 January; 115(1): 81-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11930667&dopt=Abstract
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Anti-hypertensive effect of water extract of danshen on renovascular hypertension through inhibition of the renin angiotensin system. Author(s): Kang DG, Yun YG, Ryoo JH, Lee HS. Source: The American Journal of Chinese Medicine. 2002; 30(1): 87-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12067101&dopt=Abstract
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Aqueous extract of Monascus purpureus M9011 prevents and reverses fructoseinduced hypertension in rats. Author(s): Hsieh PS, Tai YH. Source: Journal of Agricultural and Food Chemistry. 2003 July 2; 51(14): 3945-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12822928&dopt=Abstract
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Benign intracranial hypertension in association with acute lymphoblastic leukemia. Author(s): Sastry J, Karandikar SS, English MW. Source: Pediatric Hematology and Oncology. 2003 March; 20(2): 157-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12554527&dopt=Abstract
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Biofeedback and hypertension: a deja vu experience. Comments on Yucha's "Problems inherent in assessing biofeedback efficacy studies". Author(s): Blanchard EB. Source: Applied Psychophysiology and Biofeedback. 2002 March; 27(1): 107-9; Discussion 111-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12001883&dopt=Abstract
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Biofeedback of baroreflex sensitivity in patients with mild essential hypertension. Author(s): Overhaus S, Ruddel H, Curio I, Mussgay L, Scholz OB. Source: International Journal of Behavioral Medicine. 2003; 10(1): 66-78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581949&dopt=Abstract
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Blood pressure lowering effect of an olive leaf extract (Olea europaea) in L-NAME induced hypertension in rats. Author(s): Khayyal MT, el-Ghazaly MA, Abdallah DM, Nassar NN, Okpanyi SN, Kreuter MH. Source: Arzneimittel-Forschung. 2002; 52(11): 797-802. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12489249&dopt=Abstract
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Blood pressure-lowering effects of biofeedback treatment in hypertension: a metaanalysis of randomized controlled trials. Author(s): Nakao M, Yano E, Nomura S, Kuboki T. Source: Hypertens Res. 2003 January; 26(1): 37-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12661911&dopt=Abstract
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Cardiovascular, antihyperlipidemic and antioxidant effects of oleanolic and ursolic acids in experimental hypertension. Author(s): Somova LO, Nadar A, Rammanan P, Shode FO. Source: Phytomedicine : International Journal of Phytotherapy and Phytopharmacology. 2003 March; 10(2-3): 115-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12725563&dopt=Abstract
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Case study examining the efficacy of a multi-modal psychotherapeutic intervention for hypertension. Author(s): Borckardt JJ. Source: Int J Clin Exp Hypn. 2002 April; 50(2): 189-201. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11939278&dopt=Abstract
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Cerebral blood flow during plateau waves in a patient with benign intracranial hypertension--case report. Author(s): Kabeya R, Inao S, Tadokoro M, Nishino M, Yoshida J. Source: Neurol Med Chir (Tokyo). 2000 May; 40(5): 287-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11980098&dopt=Abstract
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Chronic administration of a tyrosine kinase inhibitor restores functional and morphological changes of the basilar artery during chronic hypertension. Author(s): Kitayama J, Kitazono T, Ooboshi H, Ago T, Ohgami T, Fujishima M, Ibayashi S. Source: Journal of Hypertension. 2002 November; 20(11): 2205-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12409959&dopt=Abstract
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Chronic administration of aqueous extract of Hibiscus sabdariffa attenuates hypertension and reverses cardiac hypertrophy in 2K-1C hypertensive rats. Author(s): Odigie IP, Ettarh RR, Adigun SA. Source: Journal of Ethnopharmacology. 2003 June; 86(2-3): 181-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738084&dopt=Abstract
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Comparison of different methods evaluating the functional and structural abnormalities in hypertension. Author(s): Ficzere A, Csiba L. Source: European Neurology. 2002; 48(2): 71-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12186996&dopt=Abstract
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Compliance and blood pressure control in women with hypertension. Author(s): Bobb-Liverpool B, Duff EM, Bailey EY. Source: The West Indian Medical Journal. 2002 December; 51(4): 236-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632640&dopt=Abstract
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Considering the whole patient with hypertension: the ethos of pharmaceutical care. Author(s): Coleman CA, Bleidt B. Source: Ethn Dis. 2002 Fall; 12(4): S3-72-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12477159&dopt=Abstract
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Dietary vitamin E and C supplementation prevents fructose induced hypertension in rats. Author(s): Vasdev S, Gill V, Parai S, Longerich L, Gadag V. Source: Molecular and Cellular Biochemistry. 2002 December; 241(1-2): 107-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12482032&dopt=Abstract
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Docosahexaenoic acid attenuated hypertension and vascular dementia in strokeprone spontaneously hypertensive rats. Author(s): Kimura S, Saito H, Minami M, Togashi H, Nakamura N, Ueno K, Shimamura K, Nemoto M, Parvez H. Source: Neurotoxicology and Teratology. 2002 September-October; 24(5): 683-93. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12200199&dopt=Abstract
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Drug-induced hypertension. Author(s): Handler J. Source: Journal of Clinical Hypertension (Greenwich, Conn.). 2003 January-February; 5(1): 83-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12556663&dopt=Abstract
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Effect of calcium antagonist on cerebral blood flow and oxygen metabolism in patients with hypertension and chronic major cerebral artery occlusion: a positron emission tomography study. Author(s): Ogasawara K, Noda A, Yasuda S, Kobayashi M, Yukawa H, Ogawa A. Source: Nuclear Medicine Communications. 2003 January; 24(1): 71-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12501022&dopt=Abstract
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Effect of vitamin C on pulmonary hypertension and muscularisation of pulmonary arterioles in broilers. Author(s): Xiang RP, Sun WD, Wang JY, Wang XL. Source: British Poultry Science. 2002 December; 43(5 Suppl): 705-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12555895&dopt=Abstract
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Effect of vitamin C supplementation on oxidative DNA damage in an experimental model of lead-induced hypertension. Author(s): Attri J, Dhawan V, Mahmood S, Pandhi P, Parwana HK, Nath R.
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Source: Annals of Nutrition & Metabolism. 2003; 47(6): 294-301. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14520025&dopt=Abstract •
Effects of Cudrania tricuspidata water extract on blood pressure and renal functions in NO-dependent hypertension. Author(s): Kang DG, Hur TY, Lee GM, Oh H, Kwon TO, Sohn EJ, Lee HS. Source: Life Sciences. 2002 April 19; 70(22): 2599-609. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12269387&dopt=Abstract
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Effects of docosahexaenoic acid on vascular pathology and reactivity in hypertension. Author(s): Engler MM, Engler MB, Pierson DM, Molteni LB, Molteni A. Source: Experimental Biology and Medicine (Maywood, N.J.). 2003 March; 228(3): 299307. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12626775&dopt=Abstract
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Effects of progressive muscle relaxation on blood pressure and psychosocial status for clients with essential hypertension in Taiwan. Author(s): Sheu S, Irvin BL, Lin HS, Mar CL. Source: Holistic Nursing Practice. 2003 January-February; 17(1): 41-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12597674&dopt=Abstract
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Effects of purified eicosapentaenoic and docosahexaenoic acids on glycemic control, blood pressure, and serum lipids in type 2 diabetic patients with treated hypertension. Author(s): Woodman RJ, Mori TA, Burke V, Puddey IB, Watts GF, Beilin LJ. Source: The American Journal of Clinical Nutrition. 2002 November; 76(5): 1007-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399272&dopt=Abstract
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Effects of Qigong on blood pressure, blood pressure determinants and ventilatory function in middle-aged patients with essential hypertension. Author(s): Lee MS, Lee MS, Choi ES, Chung HT. Source: The American Journal of Chinese Medicine. 2003; 31(3): 489-97. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12943180&dopt=Abstract
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Effects of Salvia miltiorrhiza extracts on rat hypoxic pulmonary hypertension, heme oxygenase-1 and nitric oxide synthase. Author(s): Chen Y, Ruan Y, Li L, Chu Y, Xu X, Wang Q, Zhou X. Source: Chin Med J (Engl). 2003 May; 116(5): 757-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12875696&dopt=Abstract
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Efficacy and safety of a therapeutic interchange from high-dose calcium channel blockers to a fixed-dose combination of amlodipine/benazepril in patients with
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moderate-to-severe hypertension. Author(s): Caro JJ, Lee K. Source: Current Hypertension Reports. 2002 December; 4(6): 417-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12419166&dopt=Abstract •
Ethnopharmacological survey of medicinal plants used for the treatment of diabetes mellitus, hypertension and cardiac diseases in the south-east region of Morocco (Tafilalet). Author(s): Eddouks M, Maghrani M, Lemhadri A, Ouahidi ML, Jouad H. Source: Journal of Ethnopharmacology. 2002 October; 82(2-3): 97-103. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12241983&dopt=Abstract
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For the patient. Are vegetarians at less risk for obesity, diabetes, and hypertension? Obesity, diabetes, hypertension, and vegetarian status among Seventh-Day Adventists in Barbados: preliminary results. Author(s): Brathwaite N, Fraser HS, Modeste N, Broome H, King R. Source: Ethn Dis. 2003 Winter; 13(1): 148. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723025&dopt=Abstract
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Hypertension and blood pressure among meat eaters, fish eaters, vegetarians and vegans in EPIC-Oxford. Author(s): Appleby PN, Davey GK, Key TJ. Source: Public Health Nutrition. 2002 October; 5(5): 645-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12372158&dopt=Abstract
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Hypertension and holistic care. Author(s): Donnelly GF. Source: Holistic Nursing Practice. 2001 July; 15(4): V. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12120498&dopt=Abstract
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Hypertension induced by St. John's Wort - a case report. Author(s): Zullino D, Borgeat F. Source: Pharmacopsychiatry. 2003 January; 36(1): 32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649772&dopt=Abstract
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Increased coronary vascular resistance cannot be reduced by inhibiting sympathetic overactivity in hypertension. Author(s): Sundell J, Laine H, Luotolahti M, Nuutila P, Knuuti J. Source: Journal of Vascular Research. 2002 September-October; 39(5): 456-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12297708&dopt=Abstract
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Increased renal vascular sensitivity to angiotensin II in hypertension is due to decreased response to prostaglandins. Author(s): Palmgren E, Widgren B, Aurell M, Herlitz H. Source: Journal of Hypertension. 2003 May; 21(5): 969-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714872&dopt=Abstract
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Increases in hypertension and blood pressure during pregnancy with increased bone lead levels. Author(s): Rothenberg SJ, Kondrashov V, Manalo M, Jiang J, Cuellar R, Garcia M, Reynoso B, Reyes S, Diaz M, Todd AC. Source: American Journal of Epidemiology. 2002 December 15; 156(12): 1079-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12480651&dopt=Abstract
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Inhaled ethyl nitrite gas for persistent pulmonary hypertension of the newborn. Author(s): Moya MP, Gow AJ, Califf RM, Goldberg RN, Stamler JS. Source: Lancet. 2002 July 13; 360(9327): 141-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12126827&dopt=Abstract
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Is lead exposure the principal cause of essential hypertension? Author(s): Gonick HC, Behari JR. Source: Medical Hypotheses. 2002 September; 59(3): 239-46. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12208146&dopt=Abstract
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Is there a role for stress management in reducing hypertension in African Americans? Author(s): Kondwani KA, Lollis CM. Source: Ethn Dis. 2001 Fall; 11(4): 788-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11763303&dopt=Abstract
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Lay beliefs about high blood pressure in a low- to middle-income urban AfricanAmerican community: an opportunity for improving hypertension control. Author(s): Wilson RP, Freeman A, Kazda MJ, Andrews TC, Berry L, Vaeth PA, Victor RG. Source: The American Journal of Medicine. 2002 January; 112(1): 26-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11812403&dopt=Abstract
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Leaf methanol extract of Bidens pilosa prevents and attenuates the hypertension induced by high-fructose diet in Wistar rats. Author(s): Dimo T, Rakotonirina SV, Tan PV, Azay J, Dongo E, Cros G. Source: Journal of Ethnopharmacology. 2002 December; 83(3): 183-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12426085&dopt=Abstract
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Lifestyle modifications to prevent hypertension. Author(s): McGuffin M.
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Source: Jama : the Journal of the American Medical Association. 2003 February 19; 289(7): 843; Author Reply 843-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588259&dopt=Abstract •
Magnesium supplementation and deoxycorticosterone acetate--salt hypertension: effect on arterial mechanical properties and on activity of endothelin-1. Author(s): Berthon N, Laurant P, Hayoz D, Fellmann D, Brunner HR, Berthelot A. Source: Canadian Journal of Physiology and Pharmacology. 2002 June; 80(6): 553-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12117304&dopt=Abstract
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Mechanism of garlic (Allium sativum) induced reduction of hypertension in 2K-1C rats: a possible mediation of Na/H exchanger isoform-1. Author(s): Al-Qattan KK, Khan I, Alnaqeeb MA, Ali M. Source: Prostaglandins, Leukotrienes, and Essential Fatty Acids. 2003 October; 69(4): 217-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12907130&dopt=Abstract
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Medically supervised water-only fasting in the treatment of borderline hypertension. Author(s): Goldhamer AC, Lisle DJ, Sultana P, Anderson SV, Parpia B, Hughes B, Campbell TC. Source: Journal of Alternative and Complementary Medicine (New York, N.Y.). 2002 October; 8(5): 643-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12470446&dopt=Abstract
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Medically supervised water-only fasting in the treatment of hypertension. Author(s): Ciurleo A, Marchese M. Source: Journal of Manipulative and Physiological Therapeutics. 2002 February; 25(2): 138-9; Author Reply 139. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11896385&dopt=Abstract
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Natural approach to hypertension. Author(s): Khosh F, Khosh M. Source: Alternative Medicine Review : a Journal of Clinical Therapeutic. 2001 December; 6(6): 590-600. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11804549&dopt=Abstract
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Nondrug interventions in hypertension prevention and control. Author(s): Labarthe D, Ayala C. Source: Cardiology Clinics. 2002 May; 20(2): 249-63. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119799&dopt=Abstract
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Non-pharmacological treatment of hypertension in women. Author(s): Costa FV.
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Source: Journal of Hypertension. 2002 May; 20 Suppl 2: S57-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12183854&dopt=Abstract •
Nutritional supplementation with Chlorella pyrenoidosa for mild to moderate hypertension. Author(s): Merchant RE, Andre CA, Sica DA. Source: Journal of Medicinal Food. 2002 Fall; 5(3): 141-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495586&dopt=Abstract
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Obesity, diabetes, hypertension, and vegetarian status among Seventh-Day Adventists in Barbados: preliminary results. Author(s): Brathwaite N, Fraser HS, Modeste N, Broome H, King R. Source: Ethn Dis. 2003 Winter; 13(1): 34-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723010&dopt=Abstract
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Osteopathic manipulative medicine in the treatment of hypertension: an alternative, conventional approach. Author(s): Spiegel AJ, Capobianco JD, Kruger A, Spinner WD. Source: Heart Disease. 2003 July-August; 5(4): 272-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12877760&dopt=Abstract
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Oxygen-15 positron-emission tomography for predicting selective delivery of a chemotherapeutic agent to hepatic cancers during angiotensin II-induced hypertension. Author(s): Koh T, Taniguchi H, Yamagishi H. Source: Cancer Chemotherapy and Pharmacology. 2003 April; 51(4): 349-58. Epub 2003 March 05. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12721763&dopt=Abstract
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Practice-based randomized controlled-comparison clinical trial of chiropractic adjustments and brief massage treatment at sites of subluxation in subjects with essential hypertension: pilot study. Author(s): Plaugher G, Long CR, Alcantara J, Silveus AD, Wood H, Lotun K, Menke JM, Meeker WC, Rowe SH. Source: Journal of Manipulative and Physiological Therapeutics. 2002 May; 25(4): 221-39. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12021741&dopt=Abstract
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Preventive effect of a chicken extract on the development of hypertension in strokeprone spontaneously hypertensive rats. Author(s): Matsumura Y, Kita S, Ono H, Kiso Y, Tanaka T. Source: Bioscience, Biotechnology, and Biochemistry. 2002 May; 66(5): 1108-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12092823&dopt=Abstract
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Promising hypotensive effect of hawthorn extract: a randomized double-blind pilot study of mild, essential hypertension. Author(s): Walker AF, Marakis G, Morris AP, Robinson PA. Source: Phytotherapy Research : Ptr. 2002 February; 16(1): 48-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11807965&dopt=Abstract
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Randomized, double-blind, placebo-controlled trial of coenzyme Q10 in isolated systolic hypertension. Author(s): Burke BE, Neuenschwander R, Olson RD. Source: Southern Medical Journal. 2001 November; 94(11): 1112-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11780680&dopt=Abstract
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Rapeseed oil ingestion and exacerbation of hypertension-related conditions in stroke prone spontaneously hypertensive rats. Author(s): Naito Y, Nagata T, Takano Y, Nagatsu T, Ohara N. Source: Toxicology. 2003 May 3; 187(2-3): 205-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699909&dopt=Abstract
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Relationship of urinary sodium/potassium excretion and calcium intake to blood pressure and prevalence of hypertension among older Chinese vegetarians. Author(s): Kwok TC, Chan TY, Woo J. Source: European Journal of Clinical Nutrition. 2003 February; 57(2): 299-304. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571663&dopt=Abstract
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Relaxation training as complementary therapy for mild hypertension control and the implications of evidence-based medicine. Author(s): Yung P, French P, Leung B. Source: Complementary Therapies in Nursing & Midwifery. 2001 May; 7(2): 59-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11855773&dopt=Abstract
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Risk of gestational hypertension in relation to folic acid supplementation during pregnancy. Author(s): Hernandez-Diaz S, Werler MM, Louik C, Mitchell AA. Source: American Journal of Epidemiology. 2002 November 1; 156(9): 806-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12396998&dopt=Abstract
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Role of blood pressure monitoring in non-pharmacological management of hypertension. Author(s): Kawano Y. Source: Blood Pressure Monitoring. 2002 February; 7(1): 51-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12040244&dopt=Abstract
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Roles of tyrosine kinase-, 1-phosphatidylinositol 3-kinase-, and mitogen-activated protein kinase-signaling pathways in ethanol-induced contractions of rat aortic smooth muscle: possible relation to alcohol-induced hypertension. Author(s): Yang ZW, Wang J, Zheng T, Altura BT, Altura BM. Source: Alcohol (Fayetteville, N.Y.). 2002 August; 28(1): 17-28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12377357&dopt=Abstract
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Serotonin-induced contraction in mesenteric resistance arteries: signaling and changes in deoxycorticosterone acetate-salt hypertension. Author(s): Watts SW. Source: Hypertension. 2002 March 1; 39(3): 825-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11897772&dopt=Abstract
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Soy milk lowers blood pressure in men and women with mild to moderate essential hypertension. Author(s): Rivas M, Garay RP, Escanero JF, Cia P Jr, Cia P, Alda JO. Source: The Journal of Nutrition. 2002 July; 132(7): 1900-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12097666&dopt=Abstract
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Status and management of hypertension in Greece: role of the adoption of a Mediterranean diet: the Attica study. Author(s): Panagiotakos DB, Pitsavos CH, Chrysohoou C, Skoumas J, Papadimitriou L, Stefanadis C, Toutouzas PK. Source: Journal of Hypertension. 2003 August; 21(8): 1483-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12872041&dopt=Abstract
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Status of lifestyle modifications in hypertension. Author(s): Chhabra MK, Lal A, Sharma KK. Source: J Indian Med Assoc. 2001 September; 99(9): 504-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12018559&dopt=Abstract
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Supplementation of L-arginine improves hypertension and lipid metabolism but not insulin resistance in diabetic rats. Author(s): Kawano T, Nomura M, Nisikado A, Nakaya Y, Ito S. Source: Life Sciences. 2003 October 24; 73(23): 3017-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14519450&dopt=Abstract
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The 10trans,12cis isomer of conjugated linoleic acid suppresses the development of hypertension in Otsuka Long-Evans Tokushima fatty rats. Author(s): Nagao K, Inoue N, Wang YM, Hirata J, Shimada Y, Nagao T, Matsui T, Yanagita T.
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Source: Biochemical and Biophysical Research Communications. 2003 June 20; 306(1): 134-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788078&dopt=Abstract •
The effect of magneto-treated blood autotransfusion on central hemodynamic values and cerebral circulation in patients with essential hypertension. Author(s): Alizade IG, Karayeva NT. Source: Saudi Med J. 2002 May; 23(5): 517-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12070571&dopt=Abstract
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The JNC 7 hypertension guidelines. Author(s): Caspi O. Source: Jama : the Journal of the American Medical Association. 2003 September 10; 290(10): 1313; Author Reply 1314-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966115&dopt=Abstract
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The nurse's role and skills in hypertension care: a review. Author(s): Bengtson A, Drevenhorn E. Source: Clinical Nurse Specialist Cns. 2003 September; 17(5): 260-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14501307&dopt=Abstract
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The role of lifestyle management in the overall treatment plan for prevention and management of hypertension. Author(s): Davis MM, Jones DW. Source: Semin Nephrol. 2002 January; 22(1): 35-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11785067&dopt=Abstract
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The sympathetic nervous system: the muse of primary hypertension. Author(s): DeQuattro V, Feng M. Source: Journal of Human Hypertension. 2002 March; 16 Suppl 1: S64-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11986898&dopt=Abstract
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The treatment of adults with essential hypertension. Author(s): Dosh SA. Source: The Journal of Family Practice. 2002 January; 51(1): 74-80. Review. Erratum In: J Fam Pract 2002 April; 51(4): 377. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11927069&dopt=Abstract
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Thermo-visual evaluation of the Yin-Tang acupuncture point for intracranial hypertension syndrome. Author(s): Ovechkin A, Kim KS, Lee JW, Lee SM.
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Source: The American Journal of Chinese Medicine. 2003; 31(3): 455-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12943176&dopt=Abstract •
Transcendental meditation, hypertension and heart disease. Author(s): King MS, Carr T, D'Cruz C. Source: Aust Fam Physician. 2002 February; 31(2): 164-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11917830&dopt=Abstract
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Treatment of Hypertension with Alternative Therapies (THAT) Study: a randomized clinical trial. Author(s): Goertz CH, Grimm RH, Svendsen K, Grandits G. Source: Journal of Hypertension. 2002 October; 20(10): 2063-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12359986&dopt=Abstract
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Why not prescribe the best drugs for hypertension now? Author(s): Wong SY, McInnes GT, MacDonald TM. Source: Journal of Human Hypertension. 2003 July; 17(7): 505-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12821958&dopt=Abstract
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Yoga practices and hypertension. Author(s): Yeolekar ME. Source: J Assoc Physicians India. 2002 May; 50(5): 631-2. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12186114&dopt=Abstract
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to hypertension; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
General Overview Age-Related Cognitive Decline Source: Healthnotes, Inc. www.healthnotes.com Angina Source: Healthnotes, Inc. www.healthnotes.com Atherosclerosis and Heart Disease Prevention Source: Prima Communications, Inc.www.personalhealthzone.com Athletic Performance Source: Healthnotes, Inc. www.healthnotes.com Bell's Palsy Source: Healthnotes, Inc. www.healthnotes.com Bone Infection Source: Integrative Medicine Communications; www.drkoop.com Canker Sores Source: Healthnotes, Inc. www.healthnotes.com Capillary Fragility Source: Healthnotes, Inc. www.healthnotes.com Cardiac Arrhythmia Source: Healthnotes, Inc. www.healthnotes.com Cardiomyopathy Source: Healthnotes, Inc. www.healthnotes.com Cardiovascular Disease Overview Source: Healthnotes, Inc. www.healthnotes.com Congestive Heart Failure Source: Healthnotes, Inc. www.healthnotes.com Diabetes Source: Prima Communications, Inc.www.personalhealthzone.com
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Diabetes Mellitus Source: Integrative Medicine Communications; www.drkoop.com Edema Source: Healthnotes, Inc. www.healthnotes.com Erectile Dysfunction Source: Healthnotes, Inc. www.healthnotes.com Fainting Source: Integrative Medicine Communications; www.drkoop.com Gastritis Source: Healthnotes, Inc. www.healthnotes.com Gestational Hypertension Source: Healthnotes, Inc. www.healthnotes.com Gout Source: Healthnotes, Inc. www.healthnotes.com Heart Attack Source: Healthnotes, Inc. www.healthnotes.com Heart Attack Source: Integrative Medicine Communications; www.drkoop.com Hepatitis Source: Healthnotes, Inc. www.healthnotes.com High Blood Pressure Source: Integrative Medicine Communications; www.drkoop.com High Cholesterol Source: Healthnotes, Inc. www.healthnotes.com High Cholesterol Source: Integrative Medicine Communications; www.drkoop.com High Cholesterol Source: Prima Communications, Inc.www.personalhealthzone.com High Homocysteine Source: Healthnotes, Inc. www.healthnotes.com High Triglycerides Source: Healthnotes, Inc. www.healthnotes.com HIV and AIDS Support Source: Healthnotes, Inc. www.healthnotes.com
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Hypercholesterolemia Source: Integrative Medicine Communications; www.drkoop.com Hyperkalemia Source: Integrative Medicine Communications; www.drkoop.com Hypertension Source: Integrative Medicine Communications; www.drkoop.com Hypertension Source: Integrative Medicine Communications; www.drkoop.com Hypertension Alternative names: High Blood Pressure Source: Prima Communications, Inc.www.personalhealthzone.com Indigestion, Heartburn, and Low Stomach Acidity Source: Healthnotes, Inc. www.healthnotes.com Insulin Resistance Syndrome Source: Healthnotes, Inc. www.healthnotes.com Liver Cirrhosis Source: Healthnotes, Inc. www.healthnotes.com Macular Degeneration Source: Healthnotes, Inc. www.healthnotes.com Menopause Source: Healthnotes, Inc. www.healthnotes.com Menopause Source: Integrative Medicine Communications; www.drkoop.com Mitral Valve Prolapse Source: Healthnotes, Inc. www.healthnotes.com Myocardial Infarction Source: Integrative Medicine Communications; www.drkoop.com Obesity Source: Integrative Medicine Communications; www.drkoop.com Osteomyelitis Source: Integrative Medicine Communications; www.drkoop.com Potassium, Excess in Blood Source: Integrative Medicine Communications; www.drkoop.com Preeclampsia Source: Healthnotes, Inc. www.healthnotes.com
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Preeclampsia Source: Integrative Medicine Communications; www.drkoop.com Pregnancy and Postpartum Support Source: Healthnotes, Inc. www.healthnotes.com Pulmonary Hypertension Source: Integrative Medicine Communications; www.drkoop.com Raynaud's Phenomenon Source: Integrative Medicine Communications; www.drkoop.com Retinopathy Source: Healthnotes, Inc. www.healthnotes.com Scleroderma Source: Integrative Medicine Communications; www.drkoop.com Stroke Source: Healthnotes, Inc. www.healthnotes.com Stroke Source: Integrative Medicine Communications; www.drkoop.com Syncope Source: Integrative Medicine Communications; www.drkoop.com Varicose Veins Source: Prima Communications, Inc.www.personalhealthzone.com •
Alternative Therapy Acupuncture Source: Healthnotes, Inc. www.healthnotes.com Apitherapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,669,00.html Chiropractic Source: Healthnotes, Inc. www.healthnotes.com Chiropractic Source: Integrative Medicine Communications; www.drkoop.com Homeovitics Alternative names: homoeovitics Source: The Canoe version of A Dictionary of Alternative-Medicine Methods, by Priorities for Health editor Jack Raso, M.S., R.D. Hyperlink: http://www.canoe.ca/AltmedDictionary/h.html
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Light Therapy Source: Healthnotes, Inc. www.healthnotes.com Mind&Body Medicine Source: Integrative Medicine Communications; www.drkoop.com Raktamoksha Source: The Canoe version of A Dictionary of Alternative-Medicine Methods, by Priorities for Health editor Jack Raso, M.S., R.D. Hyperlink: http://www.canoe.ca/AltmedDictionary/r.html Trager approach Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,741,00.html Yoga Source: Integrative Medicine Communications; www.drkoop.com •
Chinese Medicine Dilong Alternative names: Earthworm; Pheretima Source: Chinese Materia Medica Duzhong Alternative names: Eucommia Bark; Cortex Eucommiae Source: Chinese Materia Medica Fangji Alternative names: Fourstamen Stephania Root; Radix Stephaniae Tetrandrae Source: Chinese Materia Medica Gancao Jingao Alternative names: Liquorice Extract; Gancao JingaoExtractum Glycyrrhizae
Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Hyperlink: http://www.newcenturynutrition.com/cgilocal/patent_herbs_db/db.cgi?db=default&Chinese=Gancao%20Jingao&mh=10&sb =---&view_records=View+Records Gegen Alternative names: Kudzuvine Root; Radix Puerariae Source: Chinese Materia Medica Gouguye Alternative names: Chinese Holly Leaf; Folium Ilicis Cornutae Source: Chinese Materia Medica
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Gouteng Alternative names: Gambir Plant; Ramulus Uncariae cum Uncis Source: Chinese Materia Medica Luobumaye Alternative names: Dogbane Leaf; Folium Apocyni Veneti Source: Chinese Materia Medica Qingnao Jiangya Pian Alternative names: Qingnao Jiangya Tablets Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Hyperlink: http://www.newcenturynutrition.com/cgilocal/patent_herbs_db/db.cgi?db=default&Chinese=Qingnao%20Jiangya%20Pian& mh=10&sb=---&view_records=View+Records Sangjisheng Alternative names: Chinese Taxillus Herb; Herba Taxilli Source: Chinese Materia Medica Wuzhuyu Alternative names: Medicinal Evodia Fruit; Fructus Evodiae Source: Chinese Materia Medica Xiakucao Alternative names: Common Selfheal Fruit-Spike; Spica Prunellae Source: Chinese Materia Medica Yinyanghuo Alternative names: Epimedium Herb; Herba Epimedii Source: Chinese Materia Medica •
Homeopathy Argentum nitricum Source: Healthnotes, Inc. www.healthnotes.com Aurum metallicum Source: Healthnotes, Inc. www.healthnotes.com Belladonna Source: Healthnotes, Inc. www.healthnotes.com Calcarea carbonica Source: Healthnotes, Inc. www.healthnotes.com Glonoinum Source: Healthnotes, Inc. www.healthnotes.com Lachesis Source: Healthnotes, Inc. www.healthnotes.com
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Natrum muriaticum Source: Healthnotes, Inc. www.healthnotes.com Nux vomica Source: Healthnotes, Inc. www.healthnotes.com Phosphorus Source: Healthnotes, Inc. www.healthnotes.com Plumbum Source: Healthnotes, Inc. www.healthnotes.com Sanguinaria Source: Healthnotes, Inc. www.healthnotes.com •
Herbs and Supplements Acebutolol Source: Healthnotes, Inc. www.healthnotes.com ALA Source: Integrative Medicine Communications; www.drkoop.com Alpha2-Adrenergic Agonists Source: Integrative Medicine Communications; www.drkoop.com Alpha-Linolenic Acid (ALA) Source: Integrative Medicine Communications; www.drkoop.com American Ginseng Alternative names: Panax quinquefolium Source: Integrative Medicine Communications; www.drkoop.com Amiloride Source: Healthnotes, Inc. www.healthnotes.com Amino Acids Overview Source: Healthnotes, Inc. www.healthnotes.com Amlodipine Source: Healthnotes, Inc. www.healthnotes.com Ananas comosus Source: Integrative Medicine Communications; www.drkoop.com Angelica sinensis Source: Integrative Medicine Communications; www.drkoop.com Angiotensin II Receptor Blockers Source: Healthnotes, Inc. www.healthnotes.com
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Aortic Glycosaminoglycans Source: Prima Communications, Inc.www.personalhealthzone.com Arginine Source: Healthnotes, Inc. www.healthnotes.com Asian Ginseng Alternative names: Panax ginseng Source: Healthnotes, Inc. www.healthnotes.com Asian Ginseng Alternative names: Panax ginseng Source: Integrative Medicine Communications; www.drkoop.com Astragalus Alternative names: Astragalus membranaceus, Astragalus membranaceus var. mongholicus, Huang-qi, Milk-Vetch Root Source: Integrative Medicine Communications; www.drkoop.com Astragalus Source: Prima Communications, Inc.www.personalhealthzone.com Astragalus membranaceus Source: Integrative Medicine Communications; www.drkoop.com Astragalus mongholicus Alternative names: Astragalus membranaceus, Astragalus membranaceus var. mongholicus, Huang-qi, Milk-Vetch Root Source: Integrative Medicine Communications; www.drkoop.com Atenolol Source: Healthnotes, Inc. www.healthnotes.com Benazepril Source: Healthnotes, Inc. www.healthnotes.com Berberis Alternative names: Barberry; Berberis sp. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Beta-Adrenergic Blockers Source: Healthnotes, Inc. www.healthnotes.com Beta-Blockers Source: Integrative Medicine Communications; www.drkoop.com Beta-Blockers Source: Prima Communications, Inc.www.personalhealthzone.com Beta-Carotene Source: Prima Communications, Inc.www.personalhealthzone.com
Alternative Medicine 213
Betaxolol Source: Healthnotes, Inc. www.healthnotes.com Bilberry Alternative names: Vaccinium myrtillus Source: Healthnotes, Inc. www.healthnotes.com Bilberry Alternative names: Vaccinium myrtillus, European Blueberry, Huckleberry Source: Integrative Medicine Communications; www.drkoop.com Bilberry Source: Prima Communications, Inc.www.personalhealthzone.com Bisoprolol Source: Healthnotes, Inc. www.healthnotes.com Black Haw Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Blue Cohosh Alternative names: Caulophyllum thalictroides Source: Healthnotes, Inc. www.healthnotes.com Blue-Green Algae Source: Healthnotes, Inc. www.healthnotes.com Borago Alternative names: Borage; Borago officinalis Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Brahmi Alternative names: Centella asiatica , Centella, March Pennywort, Indian Pennywort, Hydrocotyle, Brahmi (Sanskrit), Luei Gong Gen (Chinese)(Note: Gotu kola should not be confused with kola nut.) Source: Integrative Medicine Communications; www.drkoop.com Brewer's Yeast Alternative names: Nutritional Yeast Source: Integrative Medicine Communications; www.drkoop.com Bromelain Source: Healthnotes, Inc. www.healthnotes.com Bromelain Alternative names: Ananas comosus, Bromelainum Source: Integrative Medicine Communications; www.drkoop.com Bromelainum Source: Integrative Medicine Communications; www.drkoop.com
214 Hypertension
Caffeine Source: Healthnotes, Inc. www.healthnotes.com Candesartan Source: Healthnotes, Inc. www.healthnotes.com Captopril Source: Healthnotes, Inc. www.healthnotes.com Carnosine Source: Healthnotes, Inc. www.healthnotes.com Carvedilol Source: Healthnotes, Inc. www.healthnotes.com Centella Alternative names: Gotu Kola; Centella asiatica (Linn.) Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Centella Source: Integrative Medicine Communications; www.drkoop.com Centella asiatica Alternative names: Centella asiatica , Centella, March Pennywort, Indian Pennywort, Hydrocotyle, Brahmi (Sanskrit), Luei Gong Gen (Chinese)(Note: Gotu kola should not be confused with kola nut.) Source: Integrative Medicine Communications; www.drkoop.com Chinese Angelica Source: Integrative Medicine Communications; www.drkoop.com Clonidine Source: Healthnotes, Inc. www.healthnotes.com Clonidine Alternative names: Catapres Source: Prima Communications, Inc.www.personalhealthzone.com Coenzyme Q10 Source: Healthnotes, Inc. www.healthnotes.com Coenzyme Q10 Source: Integrative Medicine Communications; www.drkoop.com Coenzyme Q10 (CoQ10) Source: Prima Communications, Inc.www.personalhealthzone.com Coleus Alternative names: Coleus forskohlii Source: Healthnotes, Inc. www.healthnotes.com
Alternative Medicine 215
Coleus forskohlii Source: Prima Communications, Inc.www.personalhealthzone.com CoQ10 Source: Integrative Medicine Communications; www.drkoop.com Corydalis Alternative names: Corydalis turtschaninovii, Corydalis yanhusuo Source: Healthnotes, Inc. www.healthnotes.com Crataegus Alternative names: Hawthorn; Crataegus oxyacantha L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Crataegus laevigata Source: Integrative Medicine Communications; www.drkoop.com Crataegus monogyna Source: Integrative Medicine Communications; www.drkoop.com Cyclosporine Source: Healthnotes, Inc. www.healthnotes.com Cysteine Source: Integrative Medicine Communications; www.drkoop.com Danggui Alternative names: Angelica sinensis, Chinese Angelica, Dang Gui, Danngui, Dong Qua, Tang Kuei, Tan Kue Bai zhi(Note: Dong quai should not be confused with Angelica root or Angelica seed.) Source: Integrative Medicine Communications; www.drkoop.com Dehydroepiandrosterone (DHEA) Source: Healthnotes, Inc. www.healthnotes.com DHA Source: Integrative Medicine Communications; www.drkoop.com Diltiazem Source: Healthnotes, Inc. www.healthnotes.com Diuretics Source: Healthnotes, Inc. www.healthnotes.com Docosahexaenoic Acid Source: Healthnotes, Inc. www.healthnotes.com Docosahexaenoic Acid (DHA) Source: Integrative Medicine Communications; www.drkoop.com
216 Hypertension
Dong Quai Alternative names: Angelica sinensis Source: Healthnotes, Inc. www.healthnotes.com Dong Quai Alternative names: Angelica sinensis, Chinese Angelica, Dang Gui, Danngui, Dong Qua, Tang Kuei, Tan Kue Bai zhi(Note: Dong quai should not be confused with Angelica root or Angelica seed.) Source: Integrative Medicine Communications; www.drkoop.com Dorzolamide Source: Healthnotes, Inc. www.healthnotes.com Doxazosin Source: Healthnotes, Inc. www.healthnotes.com Eicosapentaenoic Acid (EPA) Source: Integrative Medicine Communications; www.drkoop.com Eleuthero Source: Healthnotes, Inc. www.healthnotes.com Enalapril Source: Healthnotes, Inc. www.healthnotes.com EPA Source: Integrative Medicine Communications; www.drkoop.com Ephedra Source: Healthnotes, Inc. www.healthnotes.com European Blueberry Source: Integrative Medicine Communications; www.drkoop.com Felodipine Source: Healthnotes, Inc. www.healthnotes.com Fennel Source: Healthnotes, Inc. www.healthnotes.com Fiber Source: Healthnotes, Inc. www.healthnotes.com Fibric Acid Derivatives Source: Integrative Medicine Communications; www.drkoop.com Flaxseed Alternative names: Linum usitatissimum, Linseed Source: Integrative Medicine Communications; www.drkoop.com Ginkgo Biloba Source: Integrative Medicine Communications; www.drkoop.com
Alternative Medicine 217
Ginseng, American Alternative names: Panax quinquefolium Source: Integrative Medicine Communications; www.drkoop.com Ginseng, Asian Alternative names: Panax ginseng Source: Integrative Medicine Communications; www.drkoop.com Glucosamine Source: Healthnotes, Inc. www.healthnotes.com Glutathione Source: Healthnotes, Inc. www.healthnotes.com Glycyrrhiza glabra Source: Integrative Medicine Communications; www.drkoop.com Glycyrrhiza1 Alternative names: Licorice; Glycyrrhiza glabra L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Gotu Kola Alternative names: Centella asiatica Source: Healthnotes, Inc. www.healthnotes.com Gotu Kola Alternative names: Centella asiatica , Centella, March Pennywort, Indian Pennywort, Hydrocotyle, Brahmi (Sanskrit), Luei Gong Gen (Chinese)(Note: Gotu kola should not be confused with kola nut.) Source: Integrative Medicine Communications; www.drkoop.com Gotu Kola Source: Prima Communications, Inc.www.personalhealthzone.com Grape Seed Alternative names: Vitis vinifera Source: Integrative Medicine Communications; www.drkoop.com Guanfacine Source: Healthnotes, Inc. www.healthnotes.com Gymnema Alternative names: Gurmar; Gymnema sylvestre Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hawthorn Alternative names: Crataegus laevigata, Crataegus oxyacantha, Crataegus monogyna Source: Healthnotes, Inc. www.healthnotes.com
218 Hypertension
Hawthorn Alternative names: Crataegus monogyna, Crataegus laevigata Source: Integrative Medicine Communications; www.drkoop.com Hawthorn Source: Prima Communications, Inc.www.personalhealthzone.com Hawthorn Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Hawthorn Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10035,00.html Hibiscus Alternative names: Hibiscus, Roselle; Hibiscus sp. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Huang-qi Source: Integrative Medicine Communications; www.drkoop.com Huckleberry Source: Integrative Medicine Communications; www.drkoop.com Huperzine A Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10038,00.html Hydralazine Source: Healthnotes, Inc. www.healthnotes.com Hydralazine Alternative names: Apresoline Source: Prima Communications, Inc.www.personalhealthzone.com Hydrocotyle Source: Integrative Medicine Communications; www.drkoop.com Indapamide Source: Healthnotes, Inc. www.healthnotes.com Indian Pennywort Source: Integrative Medicine Communications; www.drkoop.com Irbesartan Source: Healthnotes, Inc. www.healthnotes.com
Alternative Medicine 219
Kudzu Alternative names: Pueraria lobata Source: Healthnotes, Inc. www.healthnotes.com Labetalol Source: Healthnotes, Inc. www.healthnotes.com Lemon Balm Alternative names: Melissa officinalis Source: Healthnotes, Inc. www.healthnotes.com Licorice Alternative names: Glycyrrhiza glabra, Glycyrrhiza uralensis Source: Healthnotes, Inc. www.healthnotes.com Licorice Alternative names: Glycyrrhiza glabra, Spanish Licorice Source: Integrative Medicine Communications; www.drkoop.com Linden Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Linseed Source: Integrative Medicine Communications; www.drkoop.com Linum usitatissimum Source: Integrative Medicine Communications; www.drkoop.com Liquorice Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Lisinopril Source: Healthnotes, Inc. www.healthnotes.com Loop Diuretics Source: Healthnotes, Inc. www.healthnotes.com Losartan Source: Healthnotes, Inc. www.healthnotes.com Ma Huang Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Maidenhair Tree Source: Integrative Medicine Communications; www.drkoop.com Maitake Source: Prima Communications, Inc.www.personalhealthzone.com
220 Hypertension
Marsh Pennywort Alternative names: Centella asiatica , Centella, March Pennywort, Indian Pennywort, Hydrocotyle, Brahmi (Sanskrit), Luei Gong Gen (Chinese)(Note: Gotu kola should not be confused with kola nut.) Source: Integrative Medicine Communications; www.drkoop.com Melatonin Source: Healthnotes, Inc. www.healthnotes.com Melatonin Source: Integrative Medicine Communications; www.drkoop.com Methyldopa Source: Healthnotes, Inc. www.healthnotes.com Methyldopa Alternative names: Aldomet Source: Prima Communications, Inc.www.personalhealthzone.com Metoprolol Source: Healthnotes, Inc. www.healthnotes.com Milk-Vetch Root Source: Integrative Medicine Communications; www.drkoop.com Mistletoe Alternative names: Viscum album Source: Healthnotes, Inc. www.healthnotes.com Mixed Amphetamines Source: Healthnotes, Inc. www.healthnotes.com Moexipril Source: Healthnotes, Inc. www.healthnotes.com Nadolol Source: Healthnotes, Inc. www.healthnotes.com Nettle Source: Prima Communications, Inc.www.personalhealthzone.com Nifedipine Source: Healthnotes, Inc. www.healthnotes.com Nonsteroidal Anti-inflammatory Drugs (NSAIDs) Source: Integrative Medicine Communications; www.drkoop.com Olive Leaf Alternative names: Olea europa Source: Healthnotes, Inc. www.healthnotes.com
Alternative Medicine 221
Oral Hypoglycemics Source: Prima Communications, Inc.www.personalhealthzone.com Panax Alternative names: Ginseng; Panax ginseng Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Panax ginseng Source: Integrative Medicine Communications; www.drkoop.com Panax quinquefolium Source: Integrative Medicine Communications; www.drkoop.com Phenothiazine Derivatives Source: Integrative Medicine Communications; www.drkoop.com Phenylalanine Source: Integrative Medicine Communications; www.drkoop.com Pimpinella Alternative names: Anise; Pimpinella anisum (L) Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Prazosin Source: Healthnotes, Inc. www.healthnotes.com Propranolol Source: Healthnotes, Inc. www.healthnotes.com Psyllium Alternative names: Plantago ovata, Plantago ispaghula Source: Healthnotes, Inc. www.healthnotes.com Pueraria Alternative names: Kudzu; Pueraria lobata Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Quinapril Source: Healthnotes, Inc. www.healthnotes.com Ramipril Source: Healthnotes, Inc. www.healthnotes.com Reishi Alternative names: Ganoderma lucidum Source: Healthnotes, Inc. www.healthnotes.com Ribes Alternative names: Black Currant; Ribes nigrum L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org
222 Hypertension
Selegiline Source: Healthnotes, Inc. www.healthnotes.com Siberian ginseng Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,821,00.html Silybum Alternative names: Milk Thistle; Silybum marianum (L.) Gaertn. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Spanish Licorice Source: Integrative Medicine Communications; www.drkoop.com Stevia Alternative names: Sweetleaf; Stevia rebaudiana Bertoni Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Sulfonylureas Source: Integrative Medicine Communications; www.drkoop.com Symphytum Alternative names: Comfrey; Symphytum officinale L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Tang Kuei Source: Integrative Medicine Communications; www.drkoop.com Taurine Source: Healthnotes, Inc. www.healthnotes.com Taurine Source: Prima Communications, Inc.www.personalhealthzone.com Terazosin Source: Healthnotes, Inc. www.healthnotes.com Thiazide Diuretics Source: Healthnotes, Inc. www.healthnotes.com Thiazide Diuretics Source: Integrative Medicine Communications; www.drkoop.com Thiazide Diuretics Source: Prima Communications, Inc.www.personalhealthzone.com Thioxanthene Derivatives Source: Integrative Medicine Communications; www.drkoop.com Timolol Source: Healthnotes, Inc. www.healthnotes.com
Alternative Medicine 223
Triamterene Source: Healthnotes, Inc. www.healthnotes.com Tribulus Puncture Alternative names: Puncture Vine, Goathead; Tribulus terrestris L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Tricyclic Antidepressants (TCAs) Source: Integrative Medicine Communications; www.drkoop.com Trigonella Alternative names: Fenugreek; Trigonella foenum graecum L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Triotann-S Pediatric Source: Healthnotes, Inc. www.healthnotes.com Uncaria asian Alternative names: Asian species; Uncaria sp. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Uva ursi Alternative names: Arctostaphylos uva-ursi Source: Healthnotes, Inc. www.healthnotes.com Vaccinium myrtillus Source: Integrative Medicine Communications; www.drkoop.com VacciniumB Alternative names: Bilberry; Vaccinium myrtillus L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Valerian Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Valsartan Source: Healthnotes, Inc. www.healthnotes.com Vasodilators Source: Integrative Medicine Communications; www.drkoop.com Verapamil Source: Healthnotes, Inc. www.healthnotes.com Vitis vinifera Source: Integrative Medicine Communications; www.drkoop.com Wood Betony Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca
224 Hypertension
Yarrow Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Yohimbe Alternative names: Pausinystalia yohimbe Source: Healthnotes, Inc. www.healthnotes.com Yohimbe Source: Prima Communications, Inc.www.personalhealthzone.com
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
225
CHAPTER 4. DISSERTATIONS ON HYPERTENSION Overview In this chapter, we will give you a bibliography on recent dissertations relating to hypertension. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “hypertension” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on hypertension, we have not necessarily excluded nonmedical dissertations in this bibliography.
Dissertations on Hypertension ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to hypertension. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •
A Bioanthropological Perspective of Hypertension in Arab-americans in the Metropolitan Detroit Area (michigan) by Hassoun, Rosina Jean, Phd from University of Florida, 1995, 413 pages http://wwwlib.umi.com/dissertations/fullcit/9607520
•
A Biocultural Analysis of Blood Pressure Variation among the Black Caribs and Creoles of St. Vincent, West Indies (hypertension) by Hutchinson, Janice Faye, Phd from University of Kansas, 1984, 295 pages http://wwwlib.umi.com/dissertations/fullcit/8424370
•
A Comparison of Power Spectral Analysis of Heart Rate Variability and Baroreceptor Sensitivity in Healthy, Caucasian and African American Men and Women (africanamerican, Gender Differences, Hypertension) by Horodyski, Marybeth Harman, Edd from Columbia University Teachers College, 1993, 132 pages http://wwwlib.umi.com/dissertations/fullcit/9320980
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•
A Hypertension Control Pilot Study for the African-american Elderly by Walker, Chantay Cheri, Phd from University of Alabama at Birmingham, 1998, 163 pages http://wwwlib.umi.com/dissertations/fullcit/9839864
•
A Phenomenological Approach to Compliance to Prescribed Antihypertensive Medications in Puerto Ricans by Rivera-villegas, Pedro Antonio, Phd from Southern Illinois University at Carbondale, 1995, 170 pages http://wwwlib.umi.com/dissertations/fullcit/9614971
•
A Study of the Defensive Styles Associated with Essential Hypertension and Peptic Ulcer by Belfrage, James E; Phd from York University (canada), 1978 http://wwwlib.umi.com/dissertations/fullcit/NK38481
•
A Study of the Effectiveness of a Stress Management Program on Hypertension by Bosley, Florida Mae, Phd from Washington University, 1982, 118 pages http://wwwlib.umi.com/dissertations/fullcit/8223765
•
A Study of the Impact of Level of Activity and Nutrition As It Affects Hypertension in Elderly African-americans at Two Senior Centers in Atlanta, Georgia by Maddox, Janice Helen Williams, Phd from The Union Institute, 1998, 109 pages http://wwwlib.umi.com/dissertations/fullcit/9828440
•
A Study of Three Models of Hypertension Genetic, Mineralocorticoid and Ethanolinduced by Chan, Thomas C. K; Phd from The University of British Columbia (canada), 1983 http://wwwlib.umi.com/dissertations/fullcit/NK65040
•
Acute Hypertension Inhibits Drinking Behavior but Not Vasopressin Release Stimulated by Angiotensin Ii or Hyperosmolality by Stocker, Sean David; Phd from University of Pittsburgh, 2002, 151 pages http://wwwlib.umi.com/dissertations/fullcit/3054339
•
Alcohol-induced Hepatomegaly Possible Role in Portal Hypertension by Britton, Robert S; Phd from University of Toronto (canada), 1984 http://wwwlib.umi.com/dissertations/fullcit/NK66805
•
Aldosterone Metabolism in Normal Subjects and in Patients with Benign Essential Hypertension by Grose, John H; Phd from Mcgill University (canada), 1973 http://wwwlib.umi.com/dissertations/fullcit/NK15863
•
Alterations in Endothelin Receptor Subtypes in the Pathogenesis of Hypertensioninduced Ventricular Cell Hypertrophy by Lee, Grahad Robert; Phd from Queen's University of Belfast (northern Ireland), 2002, 447 pages http://wwwlib.umi.com/dissertations/fullcit/f683937
•
Alterations in the Renal Vasculature during the Development of Hypertension by Smeda, John S; Phd from Mcmaster University (canada), 1984 http://wwwlib.umi.com/dissertations/fullcit/NK65447
•
An Assessment of the Effects of Health Education Modalities on Hypertension Clinic Outpatients. by Cryer, Dennis Craig, Phd from The University of Utah, 1975, 150 pages http://wwwlib.umi.com/dissertations/fullcit/7528871
•
An Evaluation of a Hypertension Screening and Intervention Program for High School Students. by Latham, Gail Fowler, Edd from Duke University, 1979, 210 pages http://wwwlib.umi.com/dissertations/fullcit/7922758
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•
An Examination of Social and Demographic Variables and Treatment Adherence in Male Veterans with Primary Hypertension by Totin, Martha J. Psyd from Chicago School of Professional Psychology, 2002, 110 pages http://wwwlib.umi.com/dissertations/fullcit/3049748
•
An Examination of the Efficacy of Eeg Biofeedback on the Treatment of Essential Hypertension: a Presentation and Implementation of a Comprehensive Protocol for Treating the Disorder by Peterson, Dana Timothy; Phd from Rosemead School of Psychology, Biola University, 2002, 83 pages http://wwwlib.umi.com/dissertations/fullcit/3076457
•
An Examination of the Hypothesis That Structural Changes Which Occur in Hypertension, Are a Result of the Increase in Arterial Pressure by Pang, Stephen Ching-ng; Phd from Memorial University of Newfoundland (canada), 1982 http://wwwlib.umi.com/dissertations/fullcit/NK63611
•
Ancient Environments and Modern Disease: the Case of Hypertension among Afroamericans by Wilson, Thomas Woodrow, Phd from Bowling Green State University, 1987, 204 pages http://wwwlib.umi.com/dissertations/fullcit/8728411
•
Biocultural Correlates of Pregnancy Induced Hypertension. by Poland, Marilyn Laken, Phd from Wayne State University, 1978, 92 pages http://wwwlib.umi.com/dissertations/fullcit/7816071
•
Biological Effects and Genetic Analysis of Thermosensitivity in Hypertension by Malo, Danielle; Phd from Mcgill University (canada), 1989 http://wwwlib.umi.com/dissertations/fullcit/NL52180
•
Biomedicine and Ideology: a Social History of the Conceptualization and Treatment of Essential Hypertension in the United States by Greenlee, Edwin J., Phd from Temple University, 1989, 305 pages http://wwwlib.umi.com/dissertations/fullcit/8920251
•
Blood Pressure, Blood Pressure Development and Potential Risk Factors for Hypertension with Special Reference to Metabolic Factors and Kidney Function by Kristjansson, Karl; Meddr from Goteborgs Universitet (sweden), 2002, 104 pages http://wwwlib.umi.com/dissertations/fullcit/f660673
•
Calcitonin Gene-related Peptide and Its Novel Receptors in Hypoxic Pulmonary Hypertension by Qing, Xin; , Phd from The University of Wisconsin - Madison, 2002, 172 pages http://wwwlib.umi.com/dissertations/fullcit/3060616
•
Calcium Uptake and Enzymatic Activities of Subcellular Fractions from Cardiovascular System of Normotensive and Hypertensive Rats (calcium Regulation and Hypertension) by Wei, Jiann-wu; Phd from University of Alberta (canada), 1976 http://wwwlib.umi.com/dissertations/fullcit/NK27754
•
Cardiac Remodeling and Systolic Function in Response to Hypertension (htn), Diabetes (d), and Hypertension-diabetes (h-d) by Bernal, Juan Mario; Ms from The University of Alabama at Birmingham, 2002, 61 pages http://wwwlib.umi.com/dissertations/fullcit/1411126
•
Catecholamine Synthesising Enzymes in the Programming of Hypertension by Mild Protein Restriction during Gestation by Copin, Nane; Phd from University of Southampton (united Kingdom), 2002 http://wwwlib.umi.com/dissertations/fullcit/f293089
228 Hypertension
•
Cerebrovascular Permeability in Experimental Hypertension by Nag, Sukriti; Phd from Queen's University at Kingston (canada), 1978 http://wwwlib.umi.com/dissertations/fullcit/NK37531
•
Change and Hypertension in the Population of Marakei Atoll, Kiribati by Lewis, David Eldrige, Jr., Phd from The University of Arizona, 1981, 374 pages http://wwwlib.umi.com/dissertations/fullcit/8126169
•
Characterization of Sympathetic Ganglion Sensitivity to Substance P in a Genetic and a Non-genetic Rat Model of Hypertension by Tompkins, John Daniel; Phd from East Tennessee State University, 2003, 77 pages http://wwwlib.umi.com/dissertations/fullcit/3083442
•
Childhood Hypertension - Knowledge and Health Beliefs of Sixth Graders and Their Parent(s) by Jarvis, Linda Louise, Edd from Boston University, 1986, 219 pages http://wwwlib.umi.com/dissertations/fullcit/8612174
•
Christian Meditation and Biofeedback Training As Psychotherapeutic Agents in the Treatment of Essential Hypertension by Bynum, Jack Lynn, Edd from Southwestern Baptist Theological Seminary, 1980 http://wwwlib.umi.com/dissertations/fullcit/f1026822
•
Culture Change, Stress and Epidemiological Transition in Bangladesh: an Anthropological Study of Chronic Degenerative Disorders (diabetes and Hypertension) among Rural and Urban Populations by Choudhury, Ahmed Fazle Hasan, Phd from Southern Illinois University at Carbondale, 1987, 261 pages http://wwwlib.umi.com/dissertations/fullcit/8728266
•
Determinants of Loss of Control of Hypertension by Casson, Richard Ian; Msc from Queen's University at Kingston (canada), 2002, 106 pages http://wwwlib.umi.com/dissertations/fullcit/MQ65608
•
Dietary Adherence among Rural African-american Elders with Hypertension: an Ethnographic Approach by Schoenberg, Nancy Ellen, Phd from University of Florida, 1994, 249 pages http://wwwlib.umi.com/dissertations/fullcit/9607124
•
Distribution of Regional Blood Flow and Vascular Resistance in Experimental Renal Hypertension by Allotey, John B. K; Phd from Mcgill University (canada), 1977 http://wwwlib.umi.com/dissertations/fullcit/NK33228
•
Dynamic Competition and Product Innovation Within the Prescription Antihypertensive Market by Bonk, Robert John, Phd from Philadelphia College of Pharmacy and Science, 1995, 225 pages http://wwwlib.umi.com/dissertations/fullcit/9527843
•
Effectiveness of Biofeedback Assisted Relaxation Treatment of Essential Hypertension in the Elderly by Schonfeld, Ginny M., Edd from University of Toronto (canada), 1992, 236 pages http://wwwlib.umi.com/dissertations/fullcit/NN78827
•
Effectiveness of Patient Education for Improving Compliance in Hypertension Therapy. by Lambert, Martin Lee, Jr., Phd from The University of Tennessee, 1978, 115 pages http://wwwlib.umi.com/dissertations/fullcit/7903437
Dissertations 229
•
Effects of Aerobic Fitness Level and Parental History of Hypertension on Cardiovascular Reactivity to Mental Arithmetic (psychological Stress, Blood Pressure) by Nixon, Patricia Ann, Phd from University of Pittsburgh, 1986, 79 pages http://wwwlib.umi.com/dissertations/fullcit/8701978
•
Effects of Swim Training on Blood Pressure and Other Cardiovascular Risk Factors in Individuals with Hypertension by Tanaka, Hirofumi, Phd from The University of Tennessee, 1995, 115 pages http://wwwlib.umi.com/dissertations/fullcit/9609322
•
Elastin and Elastase in the Pathogenesis of Pulmonary Hypertension in the Rat Monocrotaline Model by Todorovich-hunter, Livia; Phd from University of Toronto (canada), 1989 http://wwwlib.umi.com/dissertations/fullcit/NL54570
•
Essential Hypertension in Urban Adolescents: the Epidemiology of Obesity and Physical Fitness by Wilson, Susan Louise, Phd from Southern Methodist University, 1982, 253 pages http://wwwlib.umi.com/dissertations/fullcit/8216732
•
Essential Hypertension, Family Functioning, and Family Therapy by Duhamel, Fabie; Phd from University of Calgary (canada), 1987 http://wwwlib.umi.com/dissertations/fullcit/NL37983
•
Evaluation of the Reliability and Validity of the Hypertension Education Level Test by Martin, Barbara Clare, Edd from Southern Illinois University at Edwardsville, 1987, 71 pages http://wwwlib.umi.com/dissertations/fullcit/8725340
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Expectancy of Control Beliefs and Health Value As Predisposing Influences in Hypertension Information Preferences among Elderly Hypertensives and Nonhypertensives by Pastoriza Maldonado, Alida, Edd from Columbia University Teachers College, 1985, 174 pages http://wwwlib.umi.com/dissertations/fullcit/8510161
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Family Functioning and Hypertension in a Black Population. by Frate, Dennis Anthony, Phd from University of Illinois at Urbana-champaign, 1978, 280 pages http://wwwlib.umi.com/dissertations/fullcit/7913458
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Genetic Factors Contributing to Hypertension: with Emphasis on Hypertension in Type 2 Diabetes by Bengtsson, Kristina; Phd from Lunds Universitet (sweden), 2002, 136 pages http://wwwlib.umi.com/dissertations/fullcit/f660769
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Haemodynamic Profiling for Diagnosing and Treating Hypertension by Daniel, G. S. H; Phd from Dalhousie University (canada), 1984 http://wwwlib.umi.com/dissertations/fullcit/NK66111
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Hypertension and Social Support: the Medical Anthropology of Older, Urban Samoans by Du Bois, Barbara Constance, Phd from University of Hawaii, 1987, 447 pages http://wwwlib.umi.com/dissertations/fullcit/8812139
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Hypertension and Social Support: the Medical Anthropology of Older, Urban Samoans by Dubois, Barbara Constance, Phd from University of Hawaii, 1987 http://wwwlib.umi.com/dissertations/fullcit/f149893
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Hypertension and the Department of Transportation by Walls, George Samuel, Iii; Mph from The University of Texas Graduate Sch. of Biomedical Sci. at Galveston, 2002, 14 pages http://wwwlib.umi.com/dissertations/fullcit/1408249
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Hypertension and the Elderly: Managing Invisible Disease (compliance) by Wheeler, Robinetta Theresa, Phd from University of California, San Francisco, 1985, 216 pages http://wwwlib.umi.com/dissertations/fullcit/8513672
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Hypertension in a Defined Population: the Skaraborg Hypertension and Diabetes Project (sweden) by Bog-hansen, Erik; Phd from Lunds Universitet (sweden), 2002, 143 pages http://wwwlib.umi.com/dissertations/fullcit/f692817
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Hypertension in St. Lucia: Social and Cultural Dimensions. by Dressler, William Wymer, Phd from The University of Connecticut, 1978, 366 pages http://wwwlib.umi.com/dissertations/fullcit/7913008
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Hypertension: an Analysis of Detroit Afro-american Health Patterns (michigan) by Bailey, Eric Jon, Phd from Wayne State University, 1988, 194 pages http://wwwlib.umi.com/dissertations/fullcit/8903218
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Hypnosis Utilizing Ericksonian Techniques in the Treatment of Essential Hypertension by Kerr, Deborah Ann, Phd from University of Alberta (canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/f44565
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Hypnosis Utilizing Ericksonian Techniques in the Treatment of Essential Hypertension by Kerr, Deborah Ann; Phd from University of Alberta (canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL42916
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Immediate Early Gene Expression in the Central Nervous System in Portal Hypertension: Functional and Immunohistochemical Studies by Song, Daisheng; Phd from University of Calgary (canada), 2002, 175 pages http://wwwlib.umi.com/dissertations/fullcit/NQ77039
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In Vivo and in Vitro Studies of Cardiocytes in Genetic Hypertension by Walter, Susan Valerie; Phd from Mcgill University (canada), 1986 http://wwwlib.umi.com/dissertations/fullcit/NL38377
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Insurance Medicine: from Eyeballing to Thorough Check-up (hypertension, Aids, Immune Deficiency) by Brown, Frances Rakower, Phd from City University of New York, 1995, 210 pages http://wwwlib.umi.com/dissertations/fullcit/9530856
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Intermediate and Long Term Effects of Progressive Relaxation Training upon Senior Center Participants (hypertension) by Bloomberg, Sandra Lee, Phd from The University of Utah, 1984, 123 pages http://wwwlib.umi.com/dissertations/fullcit/8418726
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Interrelationships of the Sympathetic Nervous System, Vascular Reactivity and Electrolytes in Experimental Hypertension in Rabbits by Ayitey-smith, Edward; Phd from University of Ottawa (canada), 1971 http://wwwlib.umi.com/dissertations/fullcit/NK18121
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Job Stress and Health among Women Clerical Workers (occupational Stress, United States, Secretaries, Hypertension, Ulcers) by Balshem, Martha Levittan, Phd from Indiana University, 1985, 222 pages http://wwwlib.umi.com/dissertations/fullcit/8526982
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Lay Perceptions of Medication-taking among Women with Hypertension by Hoekelman, Margaret Campbell; Phd from University of Kentucky, 2000, 288 pages http://wwwlib.umi.com/dissertations/fullcit/9996027
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Mama Always Said: the Transmission of Health Care Beliefs among Three Generations of Rural Black Women (hypertension, South, Folk Medicine) by Randalldavid, Elizabeth Wilson, Phd from University of Florida, 1985, 237 pages http://wwwlib.umi.com/dissertations/fullcit/8523886
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Mapping Genes for Complex Traits: Obesity, Diabetes, Hypertension, and Dyslipidemia on the Pacific Island of Kosrae by Shmulewitz, Dvora; Phd from The Rockefeller University, 2002, 165 pages http://wwwlib.umi.com/dissertations/fullcit/3053194
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Mechanism of Augmented Alpha 2 Adrenergic Receptor Contraction in Aorta from Chronic Nitric Oxide Synthase Inhibited Hypertensive Rats by Carter, Rebecca W. Phd from The University of New Mexico, 2002, 142 pages http://wwwlib.umi.com/dissertations/fullcit/3058933
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Mechanisms Linking Ses to Hypertension: Findings from Three Longitudinal Studies among the Pre-retirement-age and Older Populations by Lu, Ranyan , Phd from University of Southern California, 1998, 313 pages http://wwwlib.umi.com/dissertations/fullcit/9930507
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Metabolism of Pregnenolone and Its Sulphate in Normotensive Control Subjects and Patients with Benign Essential Hypertension by Tan, Eng Lay; Phd from Mcgill University (canada), 1973 http://wwwlib.umi.com/dissertations/fullcit/NK16013
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Migration and Hypertension: an Ethnography of Disease Risk in an Urban Samoan Community (medical Ecology) by Janes, Craig Robert, Phd from Univ. of Calif., San Francisco with the Univ. of Calif., Berkeley, 1984, 406 pages http://wwwlib.umi.com/dissertations/fullcit/8425947
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Mitochondrial Dysfunction in Pulmonary Hypertension Syndrome in Broiler Chickens by Cawthon, David Randall; Phd from University of Arkansas, 2002, 149 pages http://wwwlib.umi.com/dissertations/fullcit/3067032
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Mortality, Survivorship and Longevity in American Samoa, 1950 to 1981 (cardiovascular, Hypertension, Diabetes, Obesity, Cancer) by Crews, Douglas Earl, Phd from The Pennsylvania State University, 1985, 176 pages http://wwwlib.umi.com/dissertations/fullcit/8516013
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Mutations in Wnk Kinases Cause Human Hypertension by Wilson, Frederick Hugh; Phd from Yale University, 2002, 207 pages http://wwwlib.umi.com/dissertations/fullcit/3046252
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'my Blood Boils': Folk Models of Hypertension and Compliance among Older New Orleans Black Women (louisiana) by Heurtin-roberts, Suzanne Marie, Phd from Univ. of Calif., San Francisco with the Univ. of Calif., Berkeley, 1988, 266 pages http://wwwlib.umi.com/dissertations/fullcit/8828124
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National Estimate of Cost of Illness for Hypertension and Non-persistence with Drug Therapy Using the Medical Expenditure Panel Survey by Graden, Suzanne Elaine; Phd from The Ohio State University, 2003, 183 pages http://wwwlib.umi.com/dissertations/fullcit/3088853
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Nutrition Intervention for Hypertension during Health Care Visits in Community Health Care Clinics by Mattfeldt-beman, Mildred Kay, Phd from Saint Louis University, 1992, 136 pages http://wwwlib.umi.com/dissertations/fullcit/9233814
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Observation of the Effects of Thermal Biofeedback Assisted by Autogenic Relaxation in Patients with Borderline or Mild Hypertension (biofeedback) by Chiraseveenuprapund, Anuluck, Edd from Boston University, 1994, 156 pages http://wwwlib.umi.com/dissertations/fullcit/9422504
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Patients' Knowledge and Beliefs about Hypertension and Their Reported Compliance with Treatment Regimens As Related to Blood Pressure Control. by Wolle, Joan M., Phd from University of Maryland College Park, 1977, 174 pages http://wwwlib.umi.com/dissertations/fullcit/7808197
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Peripheral Dopaminergic Mechanisms in Experimental Hypertension by Racz, Karoly; Phd from Mcgill University (canada), 1985 http://wwwlib.umi.com/dissertations/fullcit/NL31110
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Pharmacogenetic Studies of Antihypertensive Treatment: with Special Reference to the Renin-angiotensin-aldosterone System by Kurland, Lisa; Phd from Uppsala Universitet (sweden), 2002, 57 pages http://wwwlib.umi.com/dissertations/fullcit/f661009
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Physiological Factors in Micro-embolic Renal Ischemic Hypertension by Mersereau, William A; Advdeg from Mcgill University (canada), 1969 http://wwwlib.umi.com/dissertations/fullcit/NK04592
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Physiological Significance of the 5-ht(2b) and 5-ht(1b) Receptors in Deoxycorticosterone Acetate-salt Hypertension by Banes, Amy Kissiah Lynn; Phd from Michigan State University, 2002, 175 pages http://wwwlib.umi.com/dissertations/fullcit/3064200
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Preventive Health Care Planning As a Public Service in the Seattle Inner-city, with Special Reference to Hypertension Detection and Control. by Spratlen, Lois Price, Phd from University of Washington, 1976, 126 pages http://wwwlib.umi.com/dissertations/fullcit/7700624
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Program Development in Hypertension Patient Education Programs by Coyle-perkins, Geraldine Anne, Edd from Temple University, 1985, 129 pages http://wwwlib.umi.com/dissertations/fullcit/8521061
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Psychosocial Life-style Stressors and the African American Hypertensive by Cloud, Linda Diane, Phd from University of Missouri - Kansas City, 1995, 145 pages http://wwwlib.umi.com/dissertations/fullcit/9531450
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Pulmonary Disease in Scleroderma: Combined Interstitial Lung Disease and Pulmonary Hypertension and Predictors of Pulmonary Hypertension by Chang, Betty; Phd from The Johns Hopkins University, 2003, 72 pages http://wwwlib.umi.com/dissertations/fullcit/3068129
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Race, Class, and Health: Health Behavior and Hypertension in Black and White Americans by Duelberg, Sonja I., Phd from University of Illinois at Urbana-champaign, 1993, 158 pages http://wwwlib.umi.com/dissertations/fullcit/9411607
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Retinal Microvascular Abnormalities and Their Relationships with Hypertension, Cardiovascular Disease and Mortality by Wong, Tien Yin; Phd from The Johns Hopkins University, 2002, 264 pages http://wwwlib.umi.com/dissertations/fullcit/3046580
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Role Involvement, Social Identity, and Compliance with Hypertension Medical Regimens by Myjer, D'arcy Aubrey Roger, Phd from Yale University, 1988, 347 pages http://wwwlib.umi.com/dissertations/fullcit/9009417
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Role of Angiotensin in Glucocorticoid-associated Hypertension by Deng, Min; , Ms from University of Missouri - Kansas City, 2002, 87 pages http://wwwlib.umi.com/dissertations/fullcit/1410849
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Self-regard in Hypertension: a Study of Selected Quality of Life and General Attitude Variables of Hypertensive Patients by Beto, Judith A., Phd from The University of Chicago, 1990 http://wwwlib.umi.com/dissertations/fullcit/T-31177
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Socio-cultural Influences on the Pregnancy Experience: an Analysis of the Differences between Hypertensive and Normotensive Women by Lewis, Charlene Sturgess, Phd from Northwestern University, 1980, 287 pages http://wwwlib.umi.com/dissertations/fullcit/8026854
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Socioeconomic Status Configurations and the Distribution of Hypertension. by Davis, Charles George, Phd from The University of Michigan, 1975, 110 pages http://wwwlib.umi.com/dissertations/fullcit/7609380
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Sodium, the Sympathetic Nervous System and the Development of Hypertension in the Spontaneously Hypertensive Rat by Toal, Corey B; Phd from University of Toronto (canada), 1985 http://wwwlib.umi.com/dissertations/fullcit/NK66016
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Speaking of Illness: Popular Conceptions of Hypertension in American Culture by Blumhagen, Dan William, Phd from University of Washington, 1982, 270 pages http://wwwlib.umi.com/dissertations/fullcit/8218202
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Stress Inoculation Training with Hypertensive Firemen (cognitive Behavior, Relaxation Therapy) by Smith, Steve Benedict, Phd from University of Kentucky, 1985, 229 pages http://wwwlib.umi.com/dissertations/fullcit/8523934
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Stress, Social Inequality, and Culture Change: an Anthropological Approach to Human Psychophysiology (hypertension, Sociality) by Blakey, Michael Louis, Phd from University of Massachusetts, 1985, 288 pages http://wwwlib.umi.com/dissertations/fullcit/8602613
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Structural, Biophysical and Biochemical Properties of Arterial Smooth Muscle in Hypertension by Packer, Carol Subah; Phd from The University of Manitoba (canada), 1987 http://wwwlib.umi.com/dissertations/fullcit/NL37143
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Temporal Processing Deficit in Glaucoma and Ocular Hypertension by Stelmach, Lew B; Phd from University of Alberta (canada), 1985 http://wwwlib.umi.com/dissertations/fullcit/NL22931
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Test of the Effectiveness of a Hypertension Health Instruction Unit on Knowledge in a Minority Elderly Population at a Senior Citizen Center by Trowell-harris, Irene, Edd from Columbia University Teachers College, 1983, 153 pages http://wwwlib.umi.com/dissertations/fullcit/8322249
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Tetrahydrobiopterin-dependent Vasodilation Is Impaired in Experimental Hypertension by Mitchell, Brett M. Phd from Medical College of Georgia, 2003, 218 pages http://wwwlib.umi.com/dissertations/fullcit/3086344
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The Community Hypertension Management Project a Multi-center, Randomized, Controlled Clinical Trial of Computer-assisted Hypertension Management in Primary Care by Mcalister, Neil Harding; Phd from University of Toronto (canada), 1986 http://wwwlib.umi.com/dissertations/fullcit/NL29350
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The Development and Evaluation of a Group Training Program to Teach Self Control Skills to People with Hypertension by Twichell, Kristi Baatz, Phd from The University of Wisconsin - Madison, 1982, 320 pages http://wwwlib.umi.com/dissertations/fullcit/8224070
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The Diffusion of Health Information: a Study of the Dissemination Patterns of Hypertension Information. by Murdock, Marianne, Phd from Southern Illinois University at Carbondale, 1978, 178 pages http://wwwlib.umi.com/dissertations/fullcit/7817538
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The Effect of a Medication Self-care Program on Knowledge of Medication, Health Locus of Control and Self-care Behavior among Black Elderly Hypertensive Women by Harper, Doreen Connor, Phd from University of Maryland College Park, 1980, 220 pages http://wwwlib.umi.com/dissertations/fullcit/8103883
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The Effect of Hypertensive Disorders in Pregnancy on Perinatal Outcomes: a Population-based Cohort Study by Allen, Victoria Mary; Msc from University of Toronto (canada), 2002, 96 pages http://wwwlib.umi.com/dissertations/fullcit/MQ68871
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The Effect of Knowledge about Hypertension and Cultural Background on Typicality Judgments about a Scripted Event by Flynn, Janet-beth Mccann, Phd from The Catholic University of America, 1990, 155 pages http://wwwlib.umi.com/dissertations/fullcit/9107488
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The Effect of Two Methods of Patient Teaching on Selected Health Behaviors in the Treatment for Hypertension by Kneeshaw, Muriel Frances, Edd from Columbia University Teachers College, 1981, 159 pages http://wwwlib.umi.com/dissertations/fullcit/8122962
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The Effects of a Health Education Intervention Program on the Management of Hypertensive Patients by Conley, Mark Isaac, Jr., Edd from Boston University School of Education, 1982, 202 pages http://wwwlib.umi.com/dissertations/fullcit/8220914
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The Effects of Aerobic Exercise on Cardiovascular Reactivity and Baroreflex Response in Women with Parental History of Hypertension by Buckworth, Janet, Phd from University of Georgia, 1993, 170 pages http://wwwlib.umi.com/dissertations/fullcit/9329754
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The Effects of Coping Desensitization Training on the Attenuation of Blood Pressure in Essential Hypertension by Sprague, David Wayne, Phd from The Pennsylvania State University, 1988, 181 pages http://wwwlib.umi.com/dissertations/fullcit/8826822
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The Effects of Health Education on the Compliance of Hypertensive Patients to Medical Regimens by Werner, Russell Thomas, Sr., Edd from Temple University, 1980, 158 pages http://wwwlib.umi.com/dissertations/fullcit/8014571
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The Effects of Relaxation Training and Biofeedback on Essential Hypertension. by Payson, James Boyd, Edd from East Texas State University, 1976, 189 pages http://wwwlib.umi.com/dissertations/fullcit/7709634
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The Effects of Thermal Feedback with Diaphragmatic Breathing in the Treatment of White-coat Hypertension in Japan (anxiety) by Saito, Atsuko, Phd from Southern Illinois University at Carbondale, 1989, 141 pages http://wwwlib.umi.com/dissertations/fullcit/9022832
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The Efficacy of Autogenic Training and Skin Temperature Biofeedback on Hypertension by Yeager, John Micheal, Edd from Boston University School of Education, 1982, 188 pages http://wwwlib.umi.com/dissertations/fullcit/8220978
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The Influence of Exercise Intensity on Postexercise Hypotension among Middle-aged Men with High Normal to Stage I Hypertension by Zellner, Scott Richard; Phd from The University of Connecticut, 2002, 74 pages http://wwwlib.umi.com/dissertations/fullcit/3076729
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The Influence of One-kidney Goldblatt Hypertension and Cold Acclimation on Adrenergically-induced Cardiovascular and Thermoregulatory Adjustments in Rats by Fyda, Doreen M; Phd from The University of Manitoba (canada), 1987 http://wwwlib.umi.com/dissertations/fullcit/NL37277
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The Post-exercise Blood Pressure Response to Acute Exercise in Borderline Hypertensive Women by Inbar, Galit, Phd from Indiana University, 1992, 212 pages http://wwwlib.umi.com/dissertations/fullcit/9310333
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The Prospective Testing of a Psychosocial Model of Preventive Health Service Utilization in a University Population Offered Hypertension Screening by Walker, Lawrence Ronald, Phd from Temple University, 1981, 289 pages http://wwwlib.umi.com/dissertations/fullcit/8124759
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The Relationship between Knowledge and Drug Compliance among Elderly Hypertensive Patients by Barley, Linda Rose, Edd from Columbia University Teachers College, 1980, 77 pages http://wwwlib.umi.com/dissertations/fullcit/8105853
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The Role of Human Profilin in Vascular Smooth Muscle Contractility and Hypertension by Al-kheraije, Khalid Ali; Phd from The Ohio State University, 2002, 148 pages http://wwwlib.umi.com/dissertations/fullcit/3048991
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The Roles of Lithium(+), Magnesium(2+), and Sodium Ions in Bipolar Disorder and Essential Hypertension: a Multinuclear Nmr and Fluorescence Study by Williams, Nicole Marie; Phd from Loyola University of Chicago, 2002, 152 pages http://wwwlib.umi.com/dissertations/fullcit/3056455
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Two Educational Approaches to a Primary Prevention Hypertension Lesson Series: a Comparative Analysis (patient Education, Nursing, Blood Pressure) by Kirkpatrick, Mary Kinsland, Edd from North Carolina State University, 1984, 155 pages http://wwwlib.umi.com/dissertations/fullcit/8500237
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Type 2 Diabetes in a Defined Population: the Skaraborg Hypertension and Diabetes Project (sweden) by Ostgren, Carl Johan; from Lunds Universitet (sweden), 2002, 105 pages http://wwwlib.umi.com/dissertations/fullcit/f692929
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Using Traction Force Microscopy to Study the Role of Fibroblast Contractility in Hypertensive Cardiac Dysfunction by Marganski, William Alec; Phd from Boston University, 2003, 144 pages http://wwwlib.umi.com/dissertations/fullcit/3084846
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Women with Hypertension: an Ethnographic Inquiry by Harmon, Adrienne Seccia, Phd from University of Illinois at Urbana-champaign, 1993, 449 pages http://wwwlib.umi.com/dissertations/fullcit/9329053
Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. CLINICAL TRIALS AND HYPERTENSION Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning hypertension.
Recent Trials on Hypertension The following is a list of recent trials dedicated to hypertension.8 Further information on a trial is available at the Web site indicated. •
A 6-week safety & efficacy study of combination intraocular pressure-lowering therapy in patients with open-angle glaucoma or ocular hypertension Condition(s): Glaucoma, Open-Angle; Ocular Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): Alcon Research Purpose - Excerpt: To compare the intraocular pressure(IOP)-lowering efficacy of morning or evening instillations of a combination IOP-lowering therapy in patients with open-angle glaucoma or ocular hypertension. Phase(s): Phase II Study Type: Interventional Contact(s): Alcon Clinical 817-568-6747
[email protected] Web Site: http://clinicaltrials.gov/ct/show/NCT00051194
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A 6-week safety and efficacy study of Travatan compared to Xalcom in subjects with open-angle glaucoma(OAG) or ocular hypertension(OHT) Condition(s): Glaucoma, Open-Angle; Ocular Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): Alcon Research
8
These are listed at www.ClinicalTrials.gov.
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Purpose - Excerpt: To compare the safety and IOP-lowering efficacy of TRAVATAN and XALCOM in subjects with open-angle glaucoma or ocular hypertension. Phase(s): Phase IV Study Type: Interventional Contact(s): Alcon Clinical 817-568-6747
[email protected] Web Site: http://clinicaltrials.gov/ct/show/NCT00051155 •
A safety and efficacy study of Travoprost 0.004% compared to Latanoprost 0.005% in patients with open-angle glaucoma(OAG) or ocular hypertension(OHT) Condition(s): Glaucoma, Open-Angle; Ocular Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): Alcon Research Purpose - Excerpt: To evaluate the safety and IOP-lowering efficacy of Travoprost (0.004%) compared to Latanoprost (0.005%) in patients with chronic open-angle glaucoma or ocular hypertension. Phase(s): Phase IV Study Type: Interventional Contact(s): Alcon Clinical 817-568-6747
[email protected] Web Site: http://clinicaltrials.gov/ct/show/NCT00051142
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A Transition Study From Flolan(r) to Remodulin(r) in Patients with Pulmonary Arterial Hypertension Condition(s): Pulmonary Arterial Hypertension; Pulmonary Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): United Therapeutics Purpose - Excerpt: This trial is a study of Remodulin in patients with pulmonary arterial hypertension who have been transitioned from Flolan therapy. The study consists of Screening, Baseline and Treatment Phases. Patients meeting all inclusion/exclusion criteria during the Screening Phase will enter the Baseline Phase, during which baseline exercise capacity, vital signs, and clinical signs and symptoms of the disease will be assessed. After confirmation of all inclusion/exclusion criteria, patients will be assigned to study drug (Remodulin or placebo) and will enter the Treatment Phase. The Treatment Phase begins with a Dose Transition Period, during which patients will begin receiving subcutaneous study drug at a low dose determined by the patient's current dose of Flolan. The study drug dose will be increased gradually while the Flolan dose is decreased gradually over a period of up to 14 days. The dose changes will continue until Flolan therapy has been discontinued and the patient is stable on study drug. Patients who are transitioned off Flolan, who are stable on study drug will be discharged from the clinic, and will continue to receive study drug on an outpatient basis. The patient will return to the clinic at Weeks 4 and 8 for assessments. Patients will remain on study drug for 8 weeks from the first dose of study drug. At Week 8, final assessments will be conducted and the patient will be dismissed from the study. Patients who successfully complete Week 8 assessments may be offered Remodulin therapy or other therapy, at the investigator's discretion. Phase(s): Phase IV
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Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00058929 •
Inhaled Nitric Oxide and Transfusion Therapy for Patients with Sickle Cell Anemia and Secondary Pulmonary Hypertension Condition(s): Sickle Cell Anemia; Pulmonary Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: This study will test whether inhaling nitric oxide gas mixed with room air can improve pulmonary hypertension (high blood pressure in the lungs) in patients with sickle cell anemia. It is estimated that 20 to 30 percent of patients with sickle cell anemia have moderate to severe pulmonary hypertension, a disease complication associated with higher rates of illness and death. Patients with sickle cell disease 18 years of age or older may be eligible to participate in one or more parts of this three-stage study. Candidates will be screened with a medical history, physical examination, electrocardiogram, echocardiogram and blood tests. Those enrolled will undergo the following tests and procedures: Stage 1: Patients will be tested to determine the cause of pulmonary hypertension. They will have an echocardiogram (ultrasound study of the heart); a test for asthma, with measurement of arterial blood oxygen levels; oxygen breathing study with measurement of arterial blood oxygen levels; chest X-ray; computed tomography (CT) scans of the lung with and without contrast material; magnetic resonance imaging (MRI) of the heart; 6-minute walk to measure the distance covered in that time at a comfortable pace; night-hawks oxygen measurement while sleeping; blood tests for HIV, hepatitis virus, lupus and arthritis and pregnancy; pulmonary ventilation/perfusion scan with evaluation of shunt fraction to the brain and kidney; and exercise studies will be performed to determine oxygen and carbon dioxide consumption and production and to measure the anaerobic threshold. Stage 2: Patients who proceed with stage 2 will have a detailed MRI evaluation of the heart and will be admitted to the Clinical Center intensive care unit for the following procedure: A small intravenous (IV) catheter (plastic tube) is placed in the patient arm and a longer tube, called a central line, in a deeper neck or leg vein. A long thin tube is then inserted through the vein into the heart and the lung artery to measure all blood pressures in the heart and lungs directly. Following baseline measurements the following medications will be delivered for two hours each, separated by a 30 minute wash-out period. The patients is then given oxygen to breathe for 2 hours, followed by infusion of prostacyclin, a blood pressure-lowering drug, for 2 hours; and finally inhaled nitric oxide for 2 hours. A small blood sample (3 tablespoons) of blood is drawn during the nitric oxide administration. Stage 3: For patients who complete stage II or III and do not respond to NO gas as determined by a decrease in mean or systolic pulmonary artery pressure of greater than 10% from baseline or a 10% increase in 6 minute walk distance, or are unable to receive it due to technical, regulatory (no free standing home structure for storage of NO gas, etc.) or personal lifestyle issues (some patient do not want to carry two tanks of gas - oxygen and NO - or have difficulty learning how to use the NO gas system), we will offer regular exchange transfusions and home oxygen for three months with a goal of maintaining hemoglobin levels of 8-10 and hemoglobin S levels of less than 40%. The monitoring of patients receiving exchange transfusions will be the same as for the patients receiving NO gas: Measurements will include pulmonary artery pressure measured by repeat right heart catheterization, other hemodynamic
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parameters, exercise tolerance by 6-minute walk, plasma adhesion molecule levels, neutrophil and monocyte mRNA gene profiles, and circulating erythroid progenitor cell a/a hemoglobin message and protein levels. This portion of the study is to be undertaken as an outpatient. Clinical follow-up will involve bi-weekly clinic visits with the principal investigator, associate investigators, or study nurse. At these clinic visits venous blood will be obtained for hemoglobin electrophoresis (including hemoglobin F and A2), CBC, ESR, C-reactive protein and standard chemistries. Research blood, for plasma and erythrocyte reactive nitrogen species and plasma adhesion molecule levels, will be collected with total blood drawn per day not to exceed 30 mL. Protocol nurse or principal investigator will record total weekly symptoms, emergency room visits, hospital admissions, and narcotic use. Echocardiograms and 6-minute walk will be repeated at two-week intervals. 32 mL of blood will be drawn prior to the exchange transfusion and a 4 and 8 weeks for neutrophil and monocyte mRNA expression chip profiling. Patients who develop any complication of their disease (i.e. vaso-occlusive crisis, acute chest syndrome, let ulcers, priapism, avascular necrosis of the femoral hip, asthma, etc.) will be strongly encouraged to directly come to the Clinical Center's 10D ICU for evaluation and direct admission by the 10D ICU physician on-call. If they are very ill they will be instructed to either call and ambulance or go to the nearest emergency room. If they are relatively stable, patients will be instructed to call the 10D ICU and speak with the physician on-call. We will follow patients according to the NO protocol with right heart catheterization at 3 months of therapy and serial echocardiograms. The effects of exchange transfusion will be statistically analyzed separately but in a similar fashion as delineated for NO treatment. All patients will complete Stage I and II of the study prior to entering into Exchange Transfusion therapy. Patients with greater than a 10% increase in six-minute walk distance or a 10% reduction in mean or systolic pulmonary artery pressures, who want to continue Exchange Transfusion therapy will have the option of continuing therapy. In these cases, blood draws and clinical follow-up will be reduced to bi-monthly intervals and when clinically indicated. The Clinical Center will continue to pay for these clinic visits and urgent care at the Clinical Center. The Transfusion Therapy and the Clinical Center care will continue until the study has terminated (anticipated three year study duration). Our physicians and social workers will work with patients to help them obtain appropriate insurance to cover Exchange Transfusion therapy. However, it is possible that circumstances may arise that prevent the patient from continuing this therapy after the study is terminated. Alternative Therapies Patients who have enrolled in the NO or transfusion treatment arm of the study who do not respond to the treatment (defined by a 10% reduction in mean or systolic pulmonary artery pressure measured by right heart catheterization or a 10% increase in 6-minute walk distance) will be eligible to receive the alternative therapy (NO or transfusion) or other FDA approved medications. These medications may include oxygen, prostacyclin (flolan or remodulin), L-arginine, bosentan or sidenafil. We will limit the number of patients who are treated with medication other than NO or exchange transfusion to 10 subjects. Such patients will be managed at the NIH, in collaboration with their primary medical providers, according to accepted current standards of care using only FDA approved medication. The effect of such treatments on estimated pulmonary artery pressures, measured by echocardiogram, and on 6-minute walk distance will be assessed at regular intervals (every 1-3 months while on protocol) and all adverse events reported to the IRB and DSMB as defined by the current protocol. Patients maintained on alternative therapies will not have research bloods drawn, all laboratory testing will be obtained only for clinical indications. Such patients may be managed on this protocol until the protocol is terminated, the medication used becomes FDA approved specifically for use in sickle
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cell disease, the patient wishes to end participation, or the patient wishes to enroll in another study for treatment of pulmonary hypertension. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00023296 •
Magnetic Resonance Imaging for Evaluating Kidney Function Condition(s): Healthy; Renovascular Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): Warren G Magnuson Clinical Center (CC) Purpose - Excerpt: Renovascular hypertension (RVH) is a potentially curable disease affecting 0.5-5 percent of patients with hypertension. The current diagnostic work-up of RVH involves a complex algorithm which includes doppler ultrasound, captopril renography and conventional angiography. Because of the expense, risk and inconvenience of this workup, patients may not be correctly diagnosed. Advances in MR technology present the opportunity to develop a single comprehensive test. This would combine an MR angiogram that provides anatomic information about the renal arteries, and an MR renogram that provides information about the functional impact of a stenosis as a cause of hypertension. Our main purpose is to test MR renography with and without an oral angiotensin converting enzyme inhibitor (ACEI) combined with MR angiography against the reference standard of captopril radionuclide renography. Secondary goals of this study are to test whether hypoxia within ischemic kidneys affected by RVH is detectable by T2 weighted (Blood oxygen level dependent or BOLD) MRI. This is considered of value since such a test of oxygenation would further shorten and simplify the diagnostic MR test. Information gained from this study could lead to important changes in the diagnostic and pathophysiologic understanding of RVH. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006173
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Mechanism of Action of TRAVATAN 0.004% in Subjects with Glaucoma or Ocular Hypertension Condition(s): Glaucoma; Ocular Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): Alcon Research Purpose - Excerpt: The primary objective of this study is to describe the effect of TRAVATAN 0.004% Ophthalmic Solution on aqueous humor dynamics in subjects with a clinical diagnosis of open angle glaucoma (OAG) or ocular hypertension (OHT). Phase(s): Phase IV Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00061503
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Phase 3 study to evaluate IOP lowering therapy in open angle glaucoma and ocular hypertension C-01-69 Condition(s): Open-Angle Glaucoma; Ocular Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): Alcon Research Purpose - Excerpt: To compare intraocular pressure lowering effectiveness of a combination drug vs. two individual drugs dosed alone. Phase(s): Phase III Study Type: Interventional Contact(s): Alcon Call Center 1-888-451-EYES (3937) alconlabs.com Web Site: http://clinicaltrials.gov/ct/show/NCT00047515
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Phase 3 study to evaluate IOP lowering therapy in open angle glaucoma and ocular hypertension C-01-70 Condition(s): Open-Angle Glaucoma; Ocular Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): Alcon Research Purpose - Excerpt: To compare intraocular pressure lowering effectiveness of a combination drug vs. two individual drugs dosed alone. Phase(s): Phase III Study Type: Interventional Contact(s): Alcon Call Center 1-888-451-EYES (3937) alconlabs.com Web Site: http://clinicaltrials.gov/ct/show/NCT00047541
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Phase 3 study to evaluate IOP lowering therapy in open angle glaucoma and ocular hypertension C-02-41 Condition(s): Open-Angle Glaucoma; Ocular Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): Alcon Research Purpose - Excerpt: To compare intraocular pressure lowering effectiveness of a combination drug vs. two individual drugs dosed alone. Phase(s): Phase III Study Type: Interventional Contact(s): Alcon Call Center 1-888-451-EYES (3937) alconlabs.com Web Site: http://clinicaltrials.gov/ct/show/NCT00047528
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Phase II safety and efficacy study to evaluate a glaucoma therapy in open-angle glaucoma or ocular hypertension patients Condition(s): Open-Angle Glaucoma; Ocular Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): Alcon Research
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Purpose - Excerpt: The purpose of this study is to determine the safety and IOPlowering ability of a glaucoma therapy in patients with open-angle glaucoma or ocular hypertension. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00069706 •
Phase III Randomized Study of UT-15 in Patients with Primary Pulmonary Hypertension Condition(s): Pulmonary Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): FDA Office of Orphan Products Development; United Therapeutics Purpose - Excerpt: Objectives: I. Determine the safety and efficacy of UT-15 in patients with severe symptomatic primary pulmonary hypertension. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004497
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Pulmonary Hypertension--Mechanisms and Family Registry Condition(s): Lung Diseases; Hypertension, Pulmonary Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To establish a registry of primary pulmonary hypertension (PPH), a lethal disease which causes progressive obstruction of small pulmonary arteries and to investigate basic mechanisms of the disease. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005357
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Secondary Pulmonary Hypertension in Adults with Sickle Cell Anemia Condition(s): Pulmonary Hypertension; Sickle Cell Anemia Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: The purpose of this study is to determine how often people with sickle cell anemia develop pulmonary hypertension-a serious disease in which blood pressure in the artery to the lungs is elevated. Men and women 18 years of age and older with sickle cell anemia may be eligible for this study. Participants will undergo an evaluation at Howard University's Comprehensive Sickle Cell Center in Washington, D.C. or at the National Institutes of Health in Bethesda, Maryland. It will include the following: -medical history -physical examination -blood collection (no more than 50 ml., or about 1/3 cup) to confirm the diagnosis of sickle cell anemia, sickle cell trait or
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beta-thalassemia (Some blood will be stored for future research testing on sickle cell anemia.) -echocardiogram (ultrasound test of the heart) to check the pumping action of the heart and the rate at which blood travels through the tricuspid valve. Following this evaluation, a study nurse will contact participants twice a month for 2 months and then once every 3 months for the next 3 years for a telephone interview. The interview will include questions about general health and recent health-related events, such as hospitalizations or emergency room visits. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00011648 •
Treatment of Pediatric Hypertension with Altace Trial Condition(s): Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): King Pharmaceuticals; Wyeth-Ayerst Research Purpose - Excerpt: Ramipril is an ACE inhibitor that has been marketed in the US for the treatment of hypertension since 1991. It has been shown to be effective in reducing both systolic and diastolic blood pressure in adults when used once daily. ACE inhibitors are frequently used to treat hypertension in children, however ramipril has not been extensively tested in children, and information regarding the efficacy and safety would therefore be of benefit to children. This study is designed to demonstrate the efficacy and safety of ramipril in the treatment of hypertension in children ages 6 through 16 years. Phase(s): Phase IV Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00044265
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A Phase III Study of Brimonidine Tartrate Ophthalmic Solution, 0.15% in Patients with Open-Angle Glaucoma or Ocular Hypertension Condition(s): Open-Angle Glaucoma; Ocular Hypertension Study Status: This study is no longer recruiting patients. Sponsor(s): Alcon Research Purpose - Excerpt: The primary objective of this study is to compare the safety and efficacy of Brimonidine Tartrate Ophthalmic Solution, 0.15% in patients with open-angle glaucoma or ocular hypertension. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00061529
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A Study to Prevent Complications of High Blood Pressure Caused by Hepatitis in Patients with Cirrhosis Condition(s): Hypertension, Portal; Liver Cirrhosis; Esophageal and Gastric Varices
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Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); Yale University Purpose - Excerpt: Objectives: I. Evaluate the efficacy of a certain drug in preventing intestinal complications in patients with cirrhosis and high blood pressure in the hepatic portal vein. II. Evaluate vein pressure measurements to predict the development of internal bleeding. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004641 •
GenHAT--Genetics of Hypertension Associated Treatments Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension; Coronary Disease; Myocardial Infarction Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To examine whether the association between selected hypertensive genes and combined fatal coronary heart disease and nonfatal myocardial infarction in high-risk hypertensives is modified by the type of antihypertensive treatment, leading to differential risks of coronary heart disease. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006294
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Hypertension: Prediction of Biofeedback Success Condition(s): Essential Hypertension Study Status: This study is no longer recruiting patients. Sponsor(s): National Center for Complementary and Alternative Medicine (NCCAM) Purpose - Excerpt: Hypertension, present in more than 50 million Americans, increases the risk of cardiovascular disease and its associated complications. More persons are turning to alternative medicine to deal with their health problems. Biofeedback may reduce blood pressure and/or allow the reduction of antihypertensive medications in some patients, while having no adverse effects. Yet biofeedback therapy is timeintensive and technician-intensive. Therefore, it is critical to be able to predict which patients with essential hypertension are most likely to lower his/her blood pressure using these techniques. This research proposes to test three different means of predicting whether a hypertensive subject will or will not be successful in lowering his/her blood pressure using biofeedback. Sixty hypertensive subjects will be studied over a three-year period. The results of this study will enable those caring for hypertensive persons to recommend biofeedback in an individualized way, thereby promoting adherence. Phase(s): Phase I Study Type: Interventional
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00026065 •
Ocular Hypertension Treatment Study (OHTS) Condition(s): Ocular Hypertension; Glaucoma Study Status: This study is no longer recruiting patients. Sponsor(s): National Eye Institute (NEI) Purpose - Excerpt: To determine whether medical reduction of intraocular pressure prevents or delays the onset of glaucomatous visual field loss and/or optic disc damage in ocular hypertensive subjects judged to be at moderate risk for developing open-angle glaucoma. To produce natural history data to assist in identifying patients at most risk for developing open-angle glaucoma and those most likely to benefit from early medical treatment. To quantify risk factors for developing open-angle glaucoma among ocular hypertensive subjects. Phase(s): Phase III Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000125
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Phase II safety and efficacy study to evaluate a glaucoma therapy in open-angle glaucoma or ocular hypertension patients Condition(s): Open-Angle Glaucoma; Ocular Hypertension Study Status: This study is no longer recruiting patients. Sponsor(s): Alcon Research Purpose - Excerpt: To determine the safety and IOP-lowering ability of a test compound in patients with open-angle glaucoma or ocular hypertension. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00069719
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Safety and Efficacy of Sitaxsentan in the Treatment of Pulmonary Arterial Hypertension Condition(s): Pulmonary Hypertension Study Status: This study is no longer recruiting patients. Sponsor(s): ICOS-Texas Biotechnology; ICOS; Texas Biotechnology Corporation Purpose - Excerpt: This is a clinical research study designed to evaluate an investigational new medication called sitaxsentan for the treatment of pulmonary arterial hypertension (patients with NYHA functional class II, III or IV). The purpose of this study is to evaluate the safety and effectiveness of two different doses of sitaxsentan, compared to placebo (inactive treatment) for the treatment of pulmonary arterial hypertension. Patients who complete this trial may be eligible to take part in an
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extension trial (Protocol FPH01-X). Eligible patients who receive placebo in the 12-week study cross over to receive sitaxsentan for the extension trial. Phase(s): Phase II; Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00034307 •
Study of BSF 208075 evaluating exercise capacity in patients with pulmonary arterial hypertension Condition(s): Pulmonary Hypertension Study Status: This study is no longer recruiting patients. Sponsor(s): Myogen Purpose - Excerpt: The purpose of this study is to determine if treating patients suffering from moderate to severe pulmonary arterial hypertension with BSF 208075 will improve the patients' ability to exercise. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00046319
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The SILVER Study: Systolic Hypertension Interaction with Left Ventricular Remodeling Condition(s): Hypertension; Hypertrophy, Left Ventricular Study Status: This study is no longer recruiting patients. Sponsor(s): Alteon Inc. Purpose - Excerpt: The purpose of this study is to evaluate the safety and efficacy of ALT-711 in the treatment of isolated systolic hypertension in a formal study in patients with left ventricular hypertrophy. Eligible patients will be randomized to double-blind treatment once daily for 6 months with oral ALT-711 (210 mg) or placebo. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00045994
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Acupuncture and Hypertension Condition(s): Hypertension Study Status: This study is completed. Sponsor(s): National Center for Complementary and Alternative Medicine (NCCAM) Purpose - Excerpt: Although traditional Chinese medicine advocates the use of acupuncture not only to induce analgesia but also to treat essential hypertension, acupuncture's postulated antihypertensive efficacy in humans has not been subjected to rigorous Western scientific testing. Before advocating acupuncture as an effective
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complementary/alternative medicine strategy for essential hypertension, it is necessary to demonstrate that the beneficial effects of acupuncture are scientifically robust, longlasting, and explicable in terms of modern scientific mechanisms. In spontaneously hypertensive rats, acupuncture-like electrical stimulation of thinly myelinated (Group III) somatic afferents activates central endorphin (naloxone-sensitive) pathways that elicit long-lasting decreases in sympathetic nerve activity (SNA) and blood pressure. The ability to record SNA with microelectrodes in conscious humans provides a new opportunity to test this novel mechanistic hypothesis in patients undergoing electroacupuncture, a modification of the ancient technique that provides a quantifiable and reproducible stimulus to human skeletal muscle afferents. Using a randomized, double-blind placebo-controlled design, we will test the following major hypotheses: Electroacupuncture produces a long-lasting reduction in SNA, thereby providing a safe and effective complementary treatment of human hypertension. Given the enormous interest in acupuncture by our lay public, but the paucity of Western scientific data about its efficacy in cardiovascular disorders, our studies in normotensive and hypertensive humans should provide a conceptual framework for deciding whether to accept or reject the large body of Chinese (and Russian) literature advocating acupuncture as a safe and effective treatment of essential hypertension and other cardiovascular disorders (such as heart failure, and myocardial ischemia). Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00010478 •
Antecedents of Hypertension: Role of Race and Stress Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine the role of environmental stressors in the development of hypertension in Black and white school-age children from hypertensive families. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005238
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Control of Hypertension by Non-Pharmacologic Means Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension; Vascular Diseases Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine whether blood pressure could be controlled by nutritional-hygienic, non-pharmacologic means in hypertensives treated with drugs in the Hypertension Detection and Follow-up Trial (HDFP). Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000498
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Dietary Intervention Study for Hypertension (DISH) Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension; Vascular Diseases Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: The primary objective of this multicenter cooperative clinical trial was to determine if dietary modification would enable drug controlled hypertensive patients to remain at 'goal blood pressures' after antihypertensive medication was withdrawn. The proposal made use of the HDFP hypertensive population who had five years of treatment for their hypertension. Additionally, the group of investigators proposed to determine if dietary treatment would permit patients not previously adequately controlled under the HDFP program to achieve normalization of blood pressure with a combination of dietary modification and drug treatment. The study also proposed to search for predictors (i.e., levels of hormonal agents such as plasma renin activity) of responsiveness to dietary manipulation among the hypertensive population as well as to identify psychological attributes that might be of importance in managing these patients. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000497
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Effects of Rosiglitazone on Blood Vessels in Patients with High Blood Pressure and High Cholesterol Condition(s): Hypercholestrolemia; Hypertension Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Cells in the lining of blood vessels produce various substances that cause the vessels to dilate (relax) and constrict (tighten), thereby regulating blood flow. In patients with high blood pressure and high cholesterol, the blood vessels do not dilate properly. This study will investigate the effects of rosiglitazone-a drug used to improve the action of insulin in diabetic patients-on blood flow by examining its effects on endothelin (a substance that causes vessel constriction), and other substances produced by the vessel-lining cells. Adults with blood pressure recordings of 140/90 mmHg or higher on at least three separate days or with a blood cholesterol level of at least 240 mg/dl may be eligible for this study. Candidates will be screened with a medical history and physical examination, blood pressure recordings, blood and urine tests. This "crossover" study involves two separate treatment periods; that is, participants will take either rosiglitazone or placebo (an inactive look-alike pill) once a day for 8 weeks, then no drug for 4 weeks, and then the alternative treatment for the next 8 weeks. Patients will continue to take their high blood pressure medicines during the first 6 weeks of each treatment period. They will stop the medication 2 weeks before the following procedures, which are done at the end of each 8-week treatment period: Strain gauge plethysmography-A small catheter is placed through a needle into an artery at the bend of the arm for measuring blood pressure and drawing blood samples during the study. Pressure cuffs are placed on the wrist and upper arm, and a strain gauge (a rubber band device) is placed around the forearm to measure forearm blood flow. When the cuffs are inflated, blood flows into the arm, stretching the strain gauge at
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a rate proportional to the flow, and the measurement is recorded. Small doses of four drugs-acetylcholine, bradykinin, sodium nitroprusside and BQ-123-are given through the catheter. Acetylcholine slows the heart rate. Bradykinin stimulates the release of a substance that causes blood vessels to dilate and can lower blood pressure. Sodium nitroprusside causes blood vessels to dilate and is used to treat high blood pressure and heart failure. BQ-123 blocks the blood vessel-constricting activity of endothelin. Brachial ultrasound reactivity study-A baseline ultrasound image (picture produced using sound waves) of the brachial artery (artery located at the bend of the arm) is taken and blood flow measurements are recorded. Then, a pressure cuff is placed around the upper forearm, inflated for 5 minutes to stop blood flow to the forearm, and then released. Images of the artery and flow measurements are repeated. After a 15-minute rest, new baseline images are taken and flow measurements obtained. A small amount of nitroglycerin is then sprayed under the tongue and after 3 minutes, blood flow measurements and brachial artery images are recorded once more. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006071 •
Effects of Salt Intake on the Nervous Systems of Patients with Salt-Sensitive High Blood Pressure Condition(s): Hyperaldosteronism; Hypertension Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Some patients with high blood pressure can experience an increase of blood pressure by 10 percent or more by taking in salt. These patients are referred to as having "salt-sensitive" (SS) hypertension. Previous studies conducted on patients with salt sensitive hypertension suggest that their portion of the nervous system responsible for maintaining normal blood pressure (autonomic nervous system) may respond differently to salt than patients with non-salt sensitive (NSS) hypertension. This study is designed to examine the response of the nervous system to high doses of salt in patients with salt-sensitive hypertension and patients with non-salt sensitive hypertension. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001176
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Epidemiology of Hypertensive Emergency Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To test the hypotheses that hypertensive emergency was associated with non-compliance with antihypertensive medication, low level of contact with the medical care system, and alcohol abuse and cigarette smoking. Also, to describe the clinical characteristics of patients hospitalized with hypertensive emergency including morbidity, mortality, and cost, and the extent to which hypertensive emergency occured among previously diagnosed and treated hypertensives. Study Type: Observational
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005240 •
Genetic and Environmental Determinants of Hypertension Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine the pathophysiology of different types of essential hypertension by identifying the discrete effects of major genes and environmental variables as determinants of the subtypes of essential hypertension. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005149
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Guidelines for Drug Therapy of Hypertension: Closing the Loop Condition(s): Hypertension Study Status: This study is completed. Sponsor(s): Department of Veterans Affairs; Department of Veterans Affairs Health Services Research and Development Service; Stanford University Purpose - Excerpt: Hypertension is a major risk factor for heart disease and stroke. Evidence-based guidelines support the use of specific drugs for patients with specific comorbidities to maximize the decrease in cardiovascular risk; yet, many physicians do not follow these guidelines in choosing drug therapy. The goal of this project was to evaluate methods of implementing clinical practice guidelines, using hypertension as a model. We hypothesized that providing patient-specific recommendations to clinicians at the time of clinic contact with hypertensive patients would substantially improve guideline concordance of drug therapy without adversely affecting (possibly improving) blood pressure control. Our long-term goal is to develop and evaluate methods of implementing clinical practice guidelines that build on current knowledge about the most effective approaches to changing clinician behavior, and to extend those methods to other cardiovascular diseases. This project, known as ATHENA, included two major components: (1) We conducted a randomized controlled trial of patientspecific recommendations about drug therapy for hypertension, delivered to primary care clinicians at the time of primary care clinic visits. The recommendations were based on VA Hypertension Guidelines. The trial included 36 clinicians and 4500 hypertensive patients enrolled in primary care clinics at VA Palo Alto Health Care System. We compared a general intervention to an individualized intervention. Both the general and the intervention groups of clinicians received extensive guideline education, as part of a VISN-mandated hypertension guideline implementation. Clinicians randomized to the individualized intervention received, in addition, computer-generated patient-specific recommendations about drug therapy of hypertension, delivered to the clinics with the encounter forms for each visit. (2) In the 2nd major component of the study, we collaborated with Stanford Medical Informatics to develop a hypertension decision support system (ATHENA DSS). ATHENA DSS combines detailed patient information from the VA electronic medical record (VistA) with hypertension guideline knowledge based on the VA and JNC 6 hypertension guidelines. A special feature of ATHENA DSS is that the knowledge in the system can be easily browsed and updated by clinician-
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managers, so that knowledge can be kept up to date with emerging clinical trial findings about best treatments. We developed an infrastructure to implement the system in a pop-up window in the CPRS-GUI in the primary care clinics at VA Palo Alto. We also conducted an offline test of the program logic by comparing the ATHENA DSS recommendations with those made by a physician for 100 randomly selected VA patients. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00012636 •
Hypertension Detection and Follow-up Program (HDFP) Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension; Vascular Diseases Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine the effectiveness of systematic, sustained, antihypertensive therapy in reducing morbidity and mortality from hypertension in a wide spectrum of persons with elevated blood pressure in 14 communities. During its course, the trial also obtained a direct measure of the prevalence, severity, and treatment status of representative white and black populations with high blood pressure in these 14 communities, and obtained an estimate of the extent of attainable reduction of complications of high blood pressure by an organized screening and blood pressure management program. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000485
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Hypertension Prevention Trial (HPT) Feasibility Study Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension; Obesity; Vascular Diseases Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To test the feasibility and the efficacy of nutritional interventions in the primary prevention of hypertension in individuals predisposed to the development of hypertension; specifically, to test the hypothesis that reduction of weight and/or decreased sodium intake in obese individuals, or decreased sodium intake with or without increased potassium intake (in men and women, regardless of weight) would prevent the elevation of blood pressure and the incidence of hypertension. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000501
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Hypertension screening and treatment program Condition(s): Hypertension
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Study Status: This study is completed. Sponsor(s): Department of Veterans Affairs; Department of Veterans Affairs Cooperative Studies Program Purpose - Excerpt: Hypertension is one of the most common medical problems in the United States and in the VA health care system. It has been well-documented that hypertension can be effectively treated. However, there remain important unresolved clinical questions in the area of antihypertensive treatment. For example, how much is mortality affected by visit compliance, blood pressure control and type of antihypertensive agent? Or, are some regimens associated with more morbidity than others? Or, are there inexpensive regimens that are as effective as more expensive regimens? The amount of data that is available from this demonstration project (currently 6,100 patients) will help address these questions. The answers to these questions should result in better care for veterans with hypertension. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00007592 •
Hypertensive and Normal Pregnancy--Calcium Metabolism and Renin-Angiotensin SCOR in Hypertension Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension; Eclampsia; PreEclampsia Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To study calcium metabolism and the renin-angiotensin system in hypertensive and normal pregnancy. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005456
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Hypertensive Treatment and Epidemiological Analyses Condition(s): Cardiovascular Diseases; Hypertension; Heart Diseases; Coronary Disease Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine the impact of the treatment of hypertension on the epidemiological analyses of blood pressure from observational studies. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005501
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Phase IV Study of Chronic Infusional Epoprostenol for Severe Primary Pulmonary Hypertension Condition(s): Hypertension, Pulmonary Study Status: This study is completed.
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Sponsor(s): National Center for Research Resources (NCRR); Baylor College of Medicine Purpose - Excerpt: Objectives: I. Provide epoprostenol (Flolan, prostaglandin I2) by chronic infusion to patients with severe primary pulmonary hypertension for whom no alternative therapy is available. II. Obtain additional safety information on continuous infusion epoprostenol. III. Obtain additional information on economic resource health consumption. Phase(s): Phase IV Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004754 •
Polyunsaturates and KCL to Control Mild Hypertension Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension; Vascular Diseases Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To test the efficacy of omega-3 fatty acids, magnesium, calcium, and potassium supplementation in untreated mild hypertensives and magnesium and potassium supplementation in treated hypertensives. Three clinical trials were conducted in sequence over a four year period. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000511
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Prevention of Hypertension: A Randomized Trial Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension; Vascular Diseases Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine whether improved nutrition to correct overweight and high sodium intake, and regular frequent moderate rhythmic exercise to improve cardio-pulmonary fitness and to slow heart rate could lower blood pressure and prevent development of hypertension in hypertension-prone individuals. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000495
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Role of Endothelin in the Regulation of Vascular Tone in Patients with Essential Hypertension Condition(s): Hypertension Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI)
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Purpose - Excerpt: Endothelin-1 (ET-1) is a powerful vasoconstricting peptide produced predominantly by vascular endothelial cells, that exerts its effect through the interaction with specific receptors, ETA and ETB, on the underlying smooth muscle cells. Previous studies in normal subjects have demonstrated an increase in forearm blood flow after ET-1 antagonism, suggesting a physiologic role of ET-1 in the regulation of basal vascular tone. However, whether ET-1-mediated tone is increased in hypertensive patients is unknown. The main purpose of this study will be to compare the forearm vascular responses to local infusion of ET-1 receptor antagonists between normotensive and hypertensive subjects in order to assess whether ET-1-mediated basal tone is increased in patients with hypertension. In addition, we propose to study the vascular responses to local ET-1 infusion to determine whether vascular smooth muscle sensitivity to this peptide is increased in hypertensive vessels. We will use both an ETA receptor antagonist, BQ-123, and an ETB receptor antagonist, BQ-788, in order to evaluate the relative contribution of the two receptor subtypes to the regulation of vascular tone. All drugs will be infused into the brachial artery and the responses of the forearm vasculature will be measured by means of strain gauge plethysmography. Because of the relative long-lasting effect of most of the substances to be infused, the study will be performed on two separate occasions. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001527 •
Sodium Transport: Genetics and Hypertension Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Originally, to determine whether genetic alterations in pathways of sodium ion transport in the red blood cells of children could predict their risk of developing primary hypertension in adulthood. In 1992, the objective was to determine the genetic basis of interindividual variation in the risk of essential hypertension in the population at large using the Rochester Family Heart Study. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005166
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Systolic Hypertension in the Elderly Program (SHEP) Condition(s): Cardiovascular Diseases; Cerebrovascular Disorders; Heart Diseases; Hypertension Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI); National Institute on Aging (NIA) Purpose - Excerpt: The primary objective was to assess whether long-term administration of antihypertensive therapy to elderly subjects with isolated systolic hypertension reduced the combined incidence of fatal and non-fatal stroke. The secondary objectives were to evaluate: the effect of long-term antihypertensive therapy on mortality from any cause in elderly people with isolated systolic hypertension;
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possible adverse effects of chronic use of antihypertensive drug treatment in this population; the effect of therapy on indices of quality-of-life; the natural history of isolated systolic hypertension in the placebo population. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000514 •
Telmisartan vs. valsartan missed dose Condition(s): Hypertension Study Status: This study is completed. Sponsor(s): Boehringer Ingelheim Pharmaceuticals Purpose - Excerpt: The primary objectives are to demonstrate that MICARDIS(r) (telmisartan) is statistically superior to Diovan(r) (valsartan) in reducing diastolic blood pressure (DBP) following a missed dose at the end of a 6 to 8-week treatment period as measured by the 24-hour ABPM mean and to demonstrate that MICARDIS(r) is statistically superior to Diovan(r) in reducing DBP during the last 6-hours of the 24-hour dosing interval as measured by ABPM following a dose of active study medication at the end of a 6 to 8-week treatment period. Phase(s): Phase IV Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00034840
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The Role of Cyclooxygenase Activity in the Endothelial Function of Hypertensive and Hypercholesterolemic Patients Condition(s): Healthy; Hypercholesterolemia; Hypertension Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: A layer of cells called the endothelium line the walls of blood vessels. These cells produce substances that control the tone of blood vessels and thus control blood flow through the vessel. This regulating activity of the endothelium is dysfunctional in several diseases of the heart and blood vessels, including high blood pressure and high levels of cholesterol. Previous research has pointed toward a decrease in the action of nitric oxide (NO) as the cause of this abnormality. Nitric oxide is a substance produced by the cells of the endothelium that plays a role in the relaxation of blood vessels. In this project researchers plan to study blood flow through the blood vessels in patients forearms after receiving four different drugs: sodium nitroprusside, acetylcholine, L-NMMA, and aspirin. These four drugs act on the blood vessels of the forearm through different mechanisms. Acetylcholine and sodium nitroprusside are drugs that open the blood vessels of the forearm and increase blood flow through the vessel. L-NMMA is a drug that blocks production of nitric oxide (NO). Aspirin's role in controlling blood flow is unknown. Patients participating in this research study will not directly benefit from it. However, the study will contribute to researchers understanding of diseases of the blood vessels and heart.
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Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001742 •
Treatment Effects on Platelet Calcium in Hypertensive and Depressed Patients Condition(s): Depression; Hypertension Study Status: This study is not yet open for patient recruitment. Sponsor(s): Department of Veterans Affairs Medical Research Service; SmithKline Beecham Purpose - Excerpt: This study aims to determine if treatment with an SSRI antidepressant medication, paroxetine, is associated with cellular calcium response to serotonin, platelet serotonin receptors, and improvement in mood in depressed patients with or without hypertension. It is hypothesized that platelets of hypertensive patients with depressive symptomatology with be hyper-responsive to serotonin. Additionally, treatment with an SSRI antidepressant is expected to produce a down-regulation of the serotonin receptor with an associated reduction in platelet cytosolic calcium response as well as improved mood. Phase(s): Phase IV Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00018759
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Urban African-American Community Hypertension Control Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To investigate whether a health education program, developed in partnership with the community and delivered by nurse supervised community health workers (CHWs), lowered high blood pressure (HBP) in inner city African American adults. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005706
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Urinary Kallikrein and Hypertension: A Prospective Study Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine whether low total urinary kallikrein activity was prospectively associated with new hypertension onset or elevated blood pressures. Study Type: Observational Contact(s): see Web site below
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Web Site: http://clinicaltrials.gov/ct/show/NCT00005261 •
White Coat Hypertension and Antihypertensive Treatment Effect - SCOR in Hypertension Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To investigate the mechanisms of white coat hypertension and study it further as a risk factor for heart damage. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005316
Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “hypertension” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: •
For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/
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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html
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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/
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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm
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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm
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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm
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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp
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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm
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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/
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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm
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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm
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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm
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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm
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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm
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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials
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CHAPTER 6. PATENTS ON HYPERTENSION Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “hypertension” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on hypertension, we have not necessarily excluded nonmedical patents in this bibliography.
Patents on Hypertension By performing a patent search focusing on hypertension, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. The following is an 9Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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example of the type of information that you can expect to obtain from a patent search on hypertension: •
1,2,3,4-Tetrahydro-2-piperazinyl-naphthalenes for treating hypertension Inventor(s): Seiler; Max-Peter (Basel, CH) Assignee(s): Sandoz Ltd. (Basel, CH) Patent Number: 4,308,266 Date filed: September 7, 1979 Abstract: The present invention provides tetraline derivatives, useful for the treatment of hypertension, a process for their preparation and compositions containing these compounds. Excerpt(s): and ring B can contain 1, 2 or 3 double bonds... The compounds of formula I can exist in the form of enantiomers or in racemate form... In the aforementioned compounds all alkyl, alkoxy and alkanoyl groups which possess 3 or more carbon atoms, can be linear or branched. Web site: http://www.delphion.com/details?pn=US04308266__
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13-Aza prostaglandins for the treatment of glaucoma and ocular hypertension Inventor(s): Klimko; Peter G. (Fort Worth, TX) Assignee(s): Alcon Manufacturing, Ltd.. (Fort Worth, TX) Patent Number: 6,417,228 Date filed: October 29, 1999 Abstract: 13-Aza analogs of PGF.sub.2.alpha. and methods of their use in treating glaucoma and ocular hypertension are disclosed. Excerpt(s): The present invention relates to novel compounds and methods for the treatment of glaucoma and ocular hypertension. In particular, the present invention relates to the use of certain 13-aza analogs of F series prostaglandins to treat glaucoma and ocular hypertension... Glaucoma is a progressive disease which leads to optic nerve damage and, ultimately, total loss of vision. The causes of this disease have been the subject of extensive studies for many years, but are still not fully understood. The principal symptom of and/or risk factor for the disease is elevated intraocular pressure or ocular hypertension due to excess aqueous humor in the anterior chamber of the eye... The causes of aqueous humor accumulation in the anterior chamber are not fully understood. It is known that elevated intraocular pressure ("IOP") can be at least partially controlled by administering drugs which either reduce the production of aqueous humor within the eye, such as beta-blockers and carbonic anhydrase inhibitors, or increase the outflow of aqueous humor from the eye, such as miotics and sympathomimetics. Web site: http://www.delphion.com/details?pn=US06417228__
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3-Mercaptomethyl-2-oxo-1-pyrrolidine acetic acids and use for hypertension Inventor(s): Scott; William L. (Indianapolis, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 4,552,889 Date filed: June 9, 1983 Abstract: This invention provides for certain lactam derivatives, their pharmaceutical formulations, and a method of treating hypertension. Excerpt(s): The octapeptide angiotensin II is a potent pressor agent. It is formed from the decapeptide angiotensin I by the "converting enzyme" or angiotensinase. Converting enzyme has also been shown to degrade the nonapeptide bradykinin which is a vasodilator. Compounds which inhibit angiotensinase can therefore block both the formation of angiotensin II and prevent the degradation of bradykinin. By either or both of these mechanisms, inhibitors of angiotensinase are useful as antihypertensive agents both in animal models and clinically... European Patent Application Nos. 49,505 and 49,842, Biochemical And Biophysical Research Communications, 111 (1), 166 (1983), J. Med. Chem., 25, 250 (1982), and J. Med. Chem., 24, 104 (1981) all describe 3(mercaptomethyl)-N-lactamacetic acid derivatives which are said to be useful as antihypertensive agents by virtue of their ability to inhibit angiotensin converting enzyme... R.sub.3 is hydrogen or C.sub.1 -C.sub.3 alkyl. Web site: http://www.delphion.com/details?pn=US04552889__
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Aminoalkyl phenyl selenides for the treatment of hypertension and nervous system dysfunctions Inventor(s): Roberts; Steven F. (Atlanta, GA), Herman; Heath H. (Chamblee, GA), May; Sheldon W. (Atlanta, GA) Assignee(s): Georgia Tech Research Corporation (Atlanta, GA) Patent Number: 4,906,668 Date filed: October 13, 1987 Abstract: The preparation of aminoalkyl phenyl selenides and pharmaceutically acceptable salts thereof is disclosed which are useful for the treatment of hypertension and related vascular diseases and the treatment of nervous system dysfunctions. Excerpt(s): This invention relates to the synthesis of aminoalkyl phenyl selenides useful for the treatment of hypertension and nervous system dysfunctions... Phenolic arylseleno and aryl-thio compounds and other selenide and sulfide derivatives have been disclosed for use as photographic couplers. Lau, Phillip T. S., Arylthio (or seleno, or sulfonyl) Methyl-Substituted Phenolic Compounds As Photographic Couplers, Chem. Abstracts 80: 82391. Neither the structures, nor the use disclosed by Lau are related to the compositions of the present invention... May et al., U.S. Pat. No. 4,415,591 of Nov. 15, 1983, which patent is assigned in common herewith, the subject matter of which is incorporated herein by reference, discloses a method for treating hypertension involving the administration of aminoalkyl phenyl sulfide derivatives; there is also disclosed a method for evaluating the hypotensive potential of these compounds through the rate of enzymatic oxygenation by dopamine-beta-hydroxylase in the presence of an electron donor such as hexacyanoferrate (II) or ascorbic acid; and pharmaceutical compositions are also disclosed which comprise aminoalkyl phenyl sulfide or a salt thereof in amount
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effective for treatment of hypertension, a monoamine oxidase inhibitor and a nontoxic excipient. Web site: http://www.delphion.com/details?pn=US04906668__ •
Anandamide analog compositions and method of treating intraocular hypertension using same Inventor(s): Jarvinen; Tomi (Sompatie 3 I 6, 70200 Kuopio, FI), Urtti; Arto (8 Whittier Ct., Mill Valley, CA 94941), Jarvinen; Kristina (Sompatie 3 I 6, 70200 Kuopio, FI), Pate; David W. (Postbus 1397, 1000 BJ Amsterdam, NL) Assignee(s): none reported Patent Number: 5,977,180 Date filed: January 10, 1997 Abstract: Anandamide analogues useful for the treatment of intraocular hypertension, as well as ophthalmic compositions comprising the same and a cyclodextrin, and methods of use of these compounds to treat intraocular hypertension. Excerpt(s): The present invention relates to anandamide analogues useful for the treatment of intraocular hypertension, as well as ophthalmic compositions comprising the same and a cyclodextrin, and methods of use of said compositions to treat intraocular hypertension... Subjects who smoke marijuana have reduced intraocular pressure (Helper et al, J. Am. Med. Assoc., 217:1392 (1971)). The primary psychoactive ingredient in marijuana is known to be delta-9-tetrahydrocannabinol ("THC"). Human experiments involving intravenous administration of pure THC have confirmed the intraocular pressure reduction phenomenon seen with subjects who smoke marijuana (Cooler et al, South. Med. J., 70:954 (1977)). As a result, cannabinoids have been investigated as anti-glaucoma agents... However, use of systemic cannabinoids, such as THC, as anti-glaucoma agents is disadvantageous since they can cause significant adverse psychological and physiological side-effects. In addition, cannabinoids are lipophilic compounds that are very insoluble in water, thus hindering their application as topical ophthalmic pharmaceutical products. Web site: http://www.delphion.com/details?pn=US05977180__
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Antihypertensive agents and their use in treatment of hypertension Inventor(s): Trachewsky; Daniel (Oklahoma City, OK) Assignee(s): The Board of Regents of the University of Oklahoma (Norman, OK) Patent Number: 4,264,601 Date filed: June 12, 1979 Abstract: Riboflavin analogues, including both endo- and exocyclically substituted isoalloxazines which are competitive inhibitors of the enzyme flavokinase (EC 2.7.1.26) when administered in a non-toxic dosage, effectively reduce the blood pressure of a subject suffering from hypertension. Excerpt(s): The present invention relates generally to riboflavin analogues which are competitive inhibitors of the enzyme flavokinase (EC 2.7.1.26). In one aspect the invention relates to a method for reducing blood pressure of a subject suffering from
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hypertension by administering to such subject an effective, non-toxic dosage of riboflavin analogues which are competitive inhibitors of the enzyme flavokinase. More specifically, but not by way of limitation, the present invention relates to the use of endo- and exocyclically substituted isoalloxazine derivatives as antihypertensive agents for reducing the blood pressure of a subject having hypertension... It is generally known that expansion of body fluid volumes by renal retention of sodium results in an increase in the blood pressure of an individual. It is further known that certain riboflavin analogues function as competitive inhibitors of the enzyme flavokinase... I have hertofore reported at the 60th Annual Meeting of the Endocrine Society, held at Miami Beach, Florida during June 14-16, 1978, in a paper entitled "Aldosterone Stimulation of Riboflavin Incorporation into Rat Renal Flavin Coenzymes and the Effect of Inhibition by Riboflavin Analogues on Sodium Reabsorption" and published in the Journal of Clinical Investigation, Volume 62, Number 6, 1325-1333, December 1978, that the administration of aldosterone to adrenalectomized male Sprague-Dawley rats significantly increased the biosynthesis of renal flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD) in the adrenalectomized male rats. It was further reported that aldosterone significantly decreased the excretion of sodium and increased the excretion of potassium. To determine if the increased biosynthesis of the flavin coenzymes were causing the alterations in urinary sodium and potassium output by aldosterone, the riboflavin analogues, 7,8-dimethyl-10-(2'-hydroxyethyl) isoalloxazine, and 7,8-dimethyl-10-formylmethyl isoalloxazine, were administered to the animals to diminish the conversion of the riboflavin to renal flavin mononucleotide (FMN) by competitively inhibiting the enzyme flavokinase. Web site: http://www.delphion.com/details?pn=US04264601__ •
Cerebral blood outflow maintenance during intracranial hypertension Inventor(s): Pranevicius; Mindaugas (48-76-th St., Brooklyn, NY 11209), Pranevicius; Osvaldas (48-76-th St., Brooklyn, NY 11209) Assignee(s): none reported Patent Number: 6,105,582 Date filed: January 13, 1999 Abstract: Method and apparatus for detecting and treating cerebral blood vessel collapse (54) during intracranial hypertension or vasospasm by affecting cerebral venous outflow pressure (61). Venous collapse is diagnosed by lowering jugular venous bulb pressure (61) and detecting significant, progressively increasing gradient between it and ICP (60). Rising jugular venous pressure initially the collapse is terminated and then ICP starts to increase. Increasing jugular venous pressure opens collapsed vascular segments by increasing intravascular pressure. There is no increase in ICP if jugular venous pressure is maintained below value that affects ICP. During life-threatening vascular collapse caused by a plateau wave or vasospasm venous outflow pressure is temporarily increased to a level necessary to terminate collapse regardless of ICP. This is accomplished by venous occlusion catheter placed into dominant jugular vein. Catheter has highly compliant inflatable balloon operating like Starling resistor for venous outflow pressure control. Quick control of venous pressure is achieved by withdrawing/injecting fluid through catheter tip. Operation catheter is controlled by controller, which also measures ICP and possibly CBF, S.sub.jv O.sub.2. Alternative venous outflow control measures are possible.
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Excerpt(s): This invention relates to blood flow control in organs with increased compartmental- tissue pressure and collapsible vessels, specifically in the brain... The concept of critical cerebral blood flow (CBF) under the conditions of increased intracranial pressure (ICP) are well known (1,2). Studies have correlated specific levels of regional cerebral blood flow (rCBF) with reproducible clinical end points such as EEG slowing up to the point of isoelectricity. Normal rCBF of 40-60 mL/100 g/ min will maintain ion pumps, membrane potential, and the overall cellular energy pool (3). Cellular electrical failure occurs at rCBF of 15 mL/ 100 g/min (2). Decrements in rCBF below this level do not correlate with clinical end points and associated with an adverse outcome (2). From an energy standpoint, rCBF <10-12 mL/100 g/min does not support aerobic metabolism. Anaerobic glycolysis becomes predominate source of adenosine triphosphate (ATP) synthesis and intracellular acidosis steadily develops through the enhanced generation of lactate (4) If untreated, CBF <10 mL/100 g/min will induce a cascade of metabolic events, ultimately leading to cellular death. This is the CBF threshold for energy and ion homeostasis below which cellular death invariably occurs (2)... On the other hand cerebral perfusion pressure (CPP) is directly affected by ICP, because cerebral veins are exposed to cerebrospinal fluid (CSF) and passively collapse following an elevation of ICP (5). In the case of significant ICP elevation and following intracerebral vein collapse and CPP drops below its autoregulatory limits. That causes cerebral perfusion to be passively dependent from mean arterial pressure (6). Further increase in ICP ceases CBF entirely (5,7,8,9,10,11,12). Web site: http://www.delphion.com/details?pn=US06105582__ •
Combination of prostacyclin with an estrogen or progestin for the prevention and treatment of atherosclerotic vascular disease including preeclampsia and for the treatment of hypertension, and for hormone replacement therapy Inventor(s): Chwalisz; Kristof (Berlin, DE), Garfield; Robert E. (Friendswood, TX) Assignee(s): Board of Regents, The University of Texas System (Austin, TX) Patent Number: 6,613,757 Date filed: September 22, 1994 Abstract: Cardiovascular disease, including preeclampsia in pregnant women and hypertension in both women and men, are prevented or treated by administering thereto prostacyclin or a prostacyclin analog in combination with one or both of an estrogen and a progestin, which combination is also useful for HRT in peri- and postmenopausal women. Excerpt(s): This invention relates to a method for the prevention and treatment of atherosclerotic vascular disease (cardiovascular disease); for the prevention and treatment preeclampsia in pregnant women and for hormone replacement therapy in peri- and post-menopausal women, and for the treatment of hypertension in women and men... Epidemiological data indicate that approximately one half of the deaths in economically developed countries are attributable to a single major cause, viz., cardiovascular disease, including coronary heart disease, stroke and other forms of vascular disease (Green, A., Bain, C., 1993). The commonest and most lethal form of cardiovascular disease is coronary heart disease. In men, there is a continuous increase in the prevalence of cardiovascular disease after the age of 30-40 years. On the other hand, the rate of cardiovascular disease, especially coronary heart disease, is relatively low among premenopausal women but rises sharply with increasing age, suggesting that sex steroids (estrogens and progesterone) have a protective effect in women. The
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increased risk of coronary heart disease among women with bilateral oophorectomy further supports the view that steroid hormones may play a protective role with regard to cardiovascular disease... Cardiovascular disease can be prevented in postmenopausal women by hormone replacement therapy (HRT) with estrogens. The recently performed meta-analysis of 29 studies has demonstrated a reduced cardiovascular disease risk among estrogen users in 23 of these studies (Stampfer et al., 1991). There is also experimental evidence from studies in monkeys that the development of coronary atherosclerosis induced by oophorectomy and diet may be reversed by estrogen supplementation (Adams et al., 1992). On the other hand, there are no effective methods for the prevention of cardiovascular disease in man, since estrogen cannot be used because of side-effects. Web site: http://www.delphion.com/details?pn=US06613757__ •
Composition for the topical treatment of glaucoma or ocular hypertension Inventor(s): Stjernschantz; Johan W. (Uppsala, SE), Hoyng; Philip (Ke Heemstede, NL) Assignee(s): Pharmacia AB (Uppsala, SE) Patent Number: 5,079,253 Date filed: November 22, 1988 Abstract: A method for the topical treatment of glaucoma or ocular hypertension which comprises contacting the surface of the eye with a composition consisting essentially of an effective intraocular pressure reducing amount of a mixture of (a) an adrenergic agonist selected from the group consisting of epinephrine, dipivalylepinephrine, norepinephrine, phenylephrine, clonidine, isoproterenol, salbutamol, metaproterenol and terbutaline, and (b) a phosphodiesterase inhibitor selected from the group consisting of isobutylmethylxanthine, theophyllamine, Rolipram and RO-2017624, in an ophthalmically compatible carrier. Excerpt(s): The invention provides a composition for topical treatment of glaucoma or ocular hypertension comprising an effective intraocular pressure reducing amount of a mixture of an adrenergic agonist and a phosphodiesterase inhibitor in an opthalmically compatible carrier. Especially ophthalmic compositions comprising a mixture of epinephrine or dipivaloyepinephrine and isobutylmethylxanthine (IBMX) are at present preferred for use in treating glaucoma or ocular hypertension... Glaucoma is an eye disorder characterized by increased intraocular pressure, cupping of the optic disc, and visual field loss. Although the pathophysiological mechanism of open angle glaucoma is still unknown there is substantial evidence to suggest that increased intraocular pressure is detrimental to the eye, and that the increased intraocular pressure in glaucoma is the most important factor causing degenerative changes in the retina. In one particular form of glaucoma, low tension glaucoma, the actual situation may simply be that the eye is unusually sensitive to pressure and therefore damage may occur at intraocular pressure levels otherwise regarded as physiologically normal. On the other hand, some individuals may exhibit an abnormally high intraocular pressure substantially without any manifest defects in the visual field or optic disc. Such individuals are referred to as ocular hypertensives. If untreated, glaucoma almost invariably leads to blindness. The course of the disease typically is slow with progressive loss of vision. The basical principle of glaucoma treatment is to lower the intraocular pressure, either by drugs, laser treatment or surgery. The modality of treatment with drugs comprises typically instillation of pilocarpine, epinephrine, or topical beta-blocker treatment, e.g. with timolol, as well as systemically administered
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inhibitors of carbonic anhydrase, e.g. acetazolamide. Cholinesterase inhibitors such as physostigmine and echothiopate may also be employed and have an effect similar to that of pilocarpine... Although with many of these drugs the positive effects obtained are at least appreciable, concomitant adverse side-effects are often encountered which tend to diminish the usefulness of the drugs and may negatively affect patient compliance. Improvements in these respects are desirable, as well as improvements in drug efficacy. Web site: http://www.delphion.com/details?pn=US05079253__ •
Compositions and method of treating hypertension Inventor(s): Scriabine; Alexander (Ambler, PA), Stone; Clement A. (Blue Bell, PA) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 4,016,288 Date filed: August 13, 1975 Abstract: The present invention relates to a novel and useful method of treatment and a composition which is used to treat hypertension. More particularly, it relates to the administration of a composition containing (A) L-.alpha.-hydrazino-.alpha.-loweralkyl3,4-dihydroxyphenyl propionic acid or .alpha.-hydrazino-3,4-dihydroxyphenyl propionic acid or a pharmaceutically acceptable non-toxic salt of either in combination with (B) a specific class of esters of .alpha.-methyl-3,4-dihydroxyphenylalaninate or a salt thereof. Excerpt(s): It is an object of the present invention to provide a composition which more effectively treats hypertension. A further object is to provide a method of treatment which is more effective than prior art methods. A still further object is to produce a combination of drugs which is more potent than the individual components. Other objects will become apparent as the description of the invention proceeds... Or a pharmaceutically acceptable non-toxic salt thereof... In a preferred embodiment of the present invention, the "loweralkyl" group of compound (A) is methyl and the R radical is .alpha.-pivaloyloxyethyl or .alpha.-succinimidoethyl. In a still more preferred embodiment, the compound (B) is in the L or S stereo configuration. Web site: http://www.delphion.com/details?pn=US04016288__
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Compositions for treatment of ocular hypertension Inventor(s): Langham; Maurice E. (9 Candlelight Ct., Lutherville, MD 21093) Assignee(s): none reported Patent Number: 4,590,210 Date filed: April 1, 1981 Abstract: Compositions for treating ocular hypertension by topical administration containing .alpha.-methyl epinephrine, .alpha.-methyl norepinephrine, their C.sub.1 C.sub.8 alkanoyl diesters and the pharmacologically acceptable acid addition salts thereof are disclosed. Excerpt(s): The present invention relates to the treatment of ocular hypertension encountered in patients suffering from glaucoma or other ocular disorders. More
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particularly, this invention relates to compounds and compositions for effectively lowering mammalian intraocular pressure... Increased intraocular tension is caused by a disruption of the normal mechanisms regulating the pressure within the eye of a mammal. A great deal of progress has recently been made in understanding these mechanisms. It is now well established that aqueous humor drains from the eye through a sieve-like barrier into a complex network of small vessels. Ocular hypertension is directly related to rate of secretion of aqueous humor into the eye and to outflow resistance of the drainage channels, although the mechanisms of these phenomena remain to be elucidated... One of the diseases of the mammalian eye characterized by increased intraocular tension is glaucoma. Manifestations of glaucoma include hardening of the globe, excavation of the optic disc and restriction of the field of vision. Glaucoma causes blindness and, in Western man, indeed, is one of the leading causes of blindness. Web site: http://www.delphion.com/details?pn=US04590210__ •
Compounds for alleviating angiotensin related hypertension Inventor(s): Cushman; David W. (West Windsor, NJ), Ondetti; Miguel A. (Princeton, NJ) Assignee(s): E. R. Squibb & Sons, Inc. (Princeton, NJ) Patent Number: 4,339,600 Date filed: February 13, 1978 Abstract: Compounds for alleviating or reducing angiotensin related hypertension in hypertensive mammals comprising angiotensin converting enzyme inhibitors selected from a group of mercaptoacyl aminoacids. Excerpt(s): Angiotensin II is a powerful vasoconstrictor agent that has been implicated as the main causative agent in the etiology of renovascular hypertension... Angiotensin II is formed from angiotensin I by the action of angiotensin converting enzyme. Angiotensin I is a biologically inert decapeptide cleaved from the blood protein angiotensinogen by the action of the enzyme renin [Oparil et al. New England J. of Med., 291, 389-457 (1974)]. Angiotensinogen and renin are also biologically inert... Angiotensin converting enzyme is also responsible for the inactivation of bradykinin, a vasodilator agent that has been implicated in the regulation of renal function [Erdos, Circulation Research 36, 247 (1975)]. Web site: http://www.delphion.com/details?pn=US04339600__
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Cytochrome P450 arachidonic acid epoxygenase genetic mutation associated with hypertension Inventor(s): Karara; Armando (Buenos Aires, AR), Makita; Keiko (Nashville, TN), Capdevila; Jorge H. (Nashville, TN) Assignee(s): Vanderbilt University (Nashville, TN) Patent Number: 5,834,293 Date filed: September 28, 1994 Abstract: The invention provides an isolated nucleic acid encoding the rat P450 2C11 arachidonic acid epoxygenase, or a human homologue thereof, having a mutation associated with salt induced hypertension. Also provided is an isolated cell line
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expressing the epoxygenase encoded by the mutated nucleic acid, and a non-human transgenic animal having a germ line insertion of the mutated nucleic acid. Also provided is a method of screening a compound for efficacy in treating salt induced hypertension comprising administering the compound to such a non-human transgenic animal, and detecting an improvement in the animal's hypertension. The invention also provides a method of screening a human subject for a genetic predisposition to salt induced hypertension comprising detecting a mutation in a human homologue of a rat P450 2C11 arachidonic acid epoxygenase gene which affects normal epoxygenase activity. Also provided is a method of treating salt induced hypertension in a human subject associated with a genetic mutation in a human homologue of the rat P450 2C11 arachidonic acid epoxygenase gene, comprising administering to the subject a functional metabolite, or analogue thereof, produced by the human homologue of the rat P450 2C11 arachidonic acid epoxygenase. Also provided is an isolated mutated rat P450 2C11 arachidonic acid epoxygenase, or a human homologue thereof, having a mutation associated with salt induced hypertension. Excerpt(s): This invention relates to a mutation in a gene encoding Cytochrome P450 arachidonic acid epoxygenase which is associated with salt induced hypertension. The invention also relates to methods of detecting said mutation and methods of treatment of individuals afflicted with said mutation... As the precursor for prostanoid biosynthesis, arachidonic acid (AA) serves multiple and important roles in renal physiology (1,2). Studies from several laboratories have demonstrated that metabolism of this fatty acid by microsomal Cytochrome P450 generates bioactive molecules which may also be of importance to kidney function (1,3,4). The microsomal Cytochrome P450 AA epoxygenase catalyzes the NADPH-dependent metabolism of the fatty acid to a mixture of 5,6-; 8,9-; 11,12-; and 14,15-cis-epoxyeicosatrienoic acids (EETs) (3,4). The regio- and stereochemical selectivity of the AA epoxygenase is P450 isoform specific (3) and, at difference with cyclooxygenase and lipoxygenase enzymes of the arachidonate cascade, variable and more or less tissue specific (3). The demonstration that P450 participates in the in vivo metabolism of endogenous AA pools, established the epoxygenase as a member of the arachidonate cascade and suggested a functional role for the hemoprotein in the generation of bioactive eicosanoids (3)... The potent biological activities associated with several EETs has stimulated interest in defining the role that the AA epoxygenase may play in renal physiology (1,3,4). Thus, the EETs or their hydration products, the DHETs, have been shown to alter tubular Na+ and K+ fluxes (6,7), water permeability (8,9) and, to be potent systemic vasodilators (1) and enantioselective intrarenal vasoconstrictors (10). Studies with the spontaneously hypertensive rat model (1), as well as marked changes in the urinary concentration of epoxygenase metabolites during pregnancy induced hypertension (11) suggested that this pathway may be of importance for the pathophysiology of hypertension. These studies, as well as the early observation of an inhibition of cortical Na+ reabsorption by 5,6-EET (6), prompted us to investigate the effects of dietary salt in the regulation of the renal epoxygenase(s). Web site: http://www.delphion.com/details?pn=US05834293__
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Detection of hypertension using immunoreactive metabolic products Inventor(s): Kroetz; Deanna (373 Dellbrook Ave., San Francisco, CA 94131), Novak; Raymond R. (4980 Browning Dr., Orchard Lake, MI 48323), Kim; Hyesook (4683 Ravine Dr., Bloomfield Hills, MI 48301), Capdevila; Jorge H. (6549 Brownlee Dr., Nashville, TN 37205) Assignee(s): none reported Patent Number: 6,534,282 Date filed: September 4, 2001 Abstract: A method to assess hypertension by measuring the amount of free and conjugated hydroxyeicosatrienoic acids (DHETs) and metabolites of DHETs, which are metabolites of arachidonic acid (AA) epoxygenases and epoxide hydrolases, in a biological sample which contains the DHETs (using any methods including GC/MS or ELISA) is disclosed. The method further included determining the amount of molecules containing a DHET-specific epitope immunoreactive with antibodies produced against DHETs present in the sample. This amount is compared with a control sample(s). Hypertension is determined through the comparison wherein the amount of increase of free and conjugated DHETs and metabolites of DHETs in the sample isolated from an organism. The present invention also provides a method to assess catalytic activity of AA epoxygenases using immunoassays by subtracting the amounts of NADPHindependent epoxyeicosatriencic acids (EETs) from total (NADPHdependent+independent) EETs. The present invention also provides a method to decrease hepatic M epoxygenase expression including 2C23 by treatment of rats with a glucocorticoid including dexamethasone. Excerpt(s): This invention relates to a method to analyze arachidonic acid (AA)-derived products which are immunoreactive with antibodies produced against hydroxyeicosatrienoic acids (DHETs). More specifically, the present invention relates to a method which can be used to facilitate investigations of the physiological and pathophysiological roles of the metabolic products of arachidonic acid epoxygenases and epoxide hydrolases. The present invention also relates to a method to assess catalytic activity of AA epoxygenases using immunoassays and a method to decrease hepatic AA epoxygenase expression by treatment with glucocorticoids... Urinary excretion of Na.sup.+, EETs and DHETs decreased after inhibition of AA epoxygenase activity by treating rats with clotrimazole, which induced salt-sensitive and clotrimazoledependent hypertension. A salt-sensitive phenotype of the Dahl rat was associated with a lack of increases in renal AA hypoxygenases after intake of a high salt diet (10,13). A spontaneous hypertensive rat (SHR) study indicated that .omega./.omega.-1 hydroxylase activity of kidney microsomes was significantly higher than that of normotensive Witstar Kyoto rats (WKY) whereas M epoxygenase activity (EETs+DHETs) showed no difference between two strains at any age group tested (14). Urine samples were not tested. Thus it is generally concluded that the developmental phase of hypertension was linked to increases in the activity of kidney microsomal .omega./.omega.-1 hydroxylase. Indeed, recently the gene coding for CYP4A2(.omega./.omega.-1 hydroxylase) was found to be preferentially expressed in SHR (14,15)... So far, levels of urinary EETs or DHETs of SHR have not been measured or compared with those of WKY. Thus, our findings that DHET levels in urine specimens obtained from SHR is .about.56-fold higher than those of WKY and existence of free and conjugated DHETs and metabolites of DHETs in the SHR urine specimens were surprising. Our result strongly suggest that epoxide hydrolases expressed in kidney play a critical role in hypertension. Thus, measurement of total DHET levels in
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urine provides better correlation of AA epoxygenase-epoxide hydrolase activities with hypertension. Web site: http://www.delphion.com/details?pn=US06534282__ •
Determining pregnancy induced hypertension and eclampsia by immunoassay of cellular fibronectin Inventor(s): Teng; Nelson N. H. (Hillsborough, CA), Senyei; Andrew E. (Santa Ana, CA) Assignee(s): Adeza Biomedical Corporation (Sunnyvale, CA) Patent Number: 5,079,171 Date filed: January 27, 1989 Abstract: Preeclampisa, pregnancy induced hypertension (PIH) and eclampsia are determined by identifying the presence of an endothelial cell marker in a sample of blood, plasma or serum of a pregnant woman using a sandwich or competition immunoassay. Cellular fibronectin marker in a sample is determined by binding with an anti-(cellular fibronectin) antibody. Reagents for these methods are also an aspect of the invention. Excerpt(s): This invention relates to methods, reagents and kits for detection of pregnancy induced hypertension (PIH) or preeclampsia during pregnancy. In particular, this invention is directed to the determination of PIH or preeclampsia by testing whole blood, serum or plasma samples for the presence of a marker for endothelial cell injury, for example cellular fibronectin... Preeclampsia, eclampsia and pregnancy induced hypertension (PIH) are characterized by elevated blood pressure, proteinuria, and edema. The cause and nature of these disorders is only partially understood. Preeclampsia and PIH are often used to designate the same disorders. The term "preeclampsia" is used hereinafter, for purposes of clarity of explanation, not by way of limitation, to broadly include preeclampsia, pregnancy induced hypertension, and eclampsia. Although considered to be relatively rare in the United States, preeclampsia occurs worldwide in from 2 to 35 percent of pregnancies, depending on diagnostic criteria and study population. Deaths from preeclampsia are nearly equal to those from eclampsia in a recent report by Redman, C. Brit.Med.J. 296:1209-1210 (April, 1988). However, tests for these conditions are often ambiguous, and diagnosis of these conditions have often not been possible until the condition had progressed. A reliable test for early diagnosis of this condition is critically needed... A review of the role of prostaglandins in preeclampsia was published by Friedman, S. Obstet.Gynecol.71:122137 (1988). Examination of maternal fluids for metabolic markers for PIH and preeclampsia has revealed that urine levels of 2,3-dinor-6-keto PG F.sub.1.alpha. increase during this condition, Ob/Gyn Topics, 2:5 (1987). Levels of other substances in the blood have also been studied. Web site: http://www.delphion.com/details?pn=US05079171__
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Evaluation of salt sensitivity in hypertension Inventor(s): Espinel; Carlos H. (3328 "O" St., N.W., Washington, DC 20007) Assignee(s): none reported Patent Number: 5,464,018 Date filed: December 19, 1994 Abstract: A method of evaluating salt sensitivity in a hypertensive patient comprises evaluating customary salt intake and deleting from the diet any substance other than salt that might influence blood pressure, feeding the patient a diet without restriction of salt and measuring blood pressure until blood pressure becomes stabilized at the hypertensive level or, if hypertension is not seen, for about 90 days, thereafter restricting the salt intake in the diet, and gradually increasing the salt intake and measuring blood pressure to determine when the blood pressure begins to rise during the period of increasing salt intake to determine salt sensitivity that gives rise to hypertension. Excerpt(s): This invention relates to evaluation and treatment of hypertension, particularly as it relates to sodium intake of the patient... It is estimated that 40% of the United States adult population suffers from hypertension. (The American Heart Association guidelines indicate hypertension exists when the blood pressure is greater than 140/90 mm Hg.) Fifty percent of hypertension is believed linked to salt sensitivity. However, the degree to which sodium intake and hypertension are linked in causeeffect relationship has long been disputed. It is known that many hypertensive individuals respond to decrease in dietary sodium intake by decrease in blood pressure. It is also known that some hypertensive individuals fail to respond favorably to restricted salt diet. Some have recommended moderate dietary salt restriction for all patients. Restriction of salt is not without danger, particularly during hot weather or strenuous exercise. The failure of salt restrictions to control hypertension most likely arises from indiscriminate implementation of the restricted salt/sodium diet. Prediction of the effect of restriction of sodium intake in any particular patient may be an important factor in determining treatment protocol for the patient. Previously a patient was deemed salt-sensitive if (SBP-DBP).div.3+(DBP) where SBP is systolic blood pressure and DBP is diastolic blood pressure showed >10 mm Hg increase in response to an administration of sodium chloride in amounts higher than the customary intake subsequent to administration of sodium chloride after depletion. (Causes of depletion may include administration of diuretic agents or severe dietary restrictions.) Methods of evaluation using these criteria were not found to be readily applicable. Failure to reflect customary habits and diet were probably factors that decreased applicability of the evaluative methods previously used... It is the purpose of this invention to provide means for identifying patients that suffer from hypertension related to salt sensitivity. It is also a purpose of this invention to provide guidelines for choosing treatment modalities for patients suffering from hypertension. By methods of the invention it is possible to determine, not only the presence, but also the degree of salt sensitivity. Web site: http://www.delphion.com/details?pn=US05464018__
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Extracts of mixed arctium lappa L., carrot and whole radish for treating hypertension, constipation and detoxification Inventor(s): Xu; Dong (Jiangxi, CN), Shi; Yuan (Little Neck, NY), Yang; Yongsen (Jiangxi, CN) Assignee(s): Chengzhi Life Science Company, Ltd. (Beijing, CN) Patent Number: 6,428,822 Date filed: April 3, 2001 Abstract: A mixed substance for treating hypertension, constipation, detoxification, boost immune system produced by extracting arctium lappa L., carrot, and whole radish with water one or two hours at temperature 70.degree. C. 100.degree. C. under agitating, separated the extracts and solid by-products, vacuum condensed the extracts, then at low temperature lyophilized condensed extracts to powder, encapsulated powder or pressed powder to tablet. Patient taking a daily dosage of this vegetable medicine have shown greatly improved healthy condition. Excerpt(s): This invention relates to vegetable medicine, specifically to cure sickness and improve healthy condition... This invention relates to extracts of arctium lappa L., carrot and whole radish (radish and radish leaves) substance having anti hypertension, detoxification and treating constipation properties. Hypertension is the medical term for high blood pressure. It is defined in an adult as a blood pressure greater than or equal to 140 mmHg systolic pressure or greater than or equal to 90 mmHg diastolic pressure. Blood pressure is measured in millimeters of mercury (mmHg). High blood pressure directly increases the risk of coronary heart disease (which leads to heart attack) and stroke, especially along with other risk factors. High blood pressure can occur in children or adults, but it's more common among people over age 35. Medical science does not understand why most cases of high blood pressure occur, it's hard to say how to prevent it... Current pharmaceutical treatments for essential hypertension include diuretics, beta-blockers, ACE inhibitors, angaotensin converting enzyme inhibitors, thiazid and calcium antagonists. Some of them were patented, such as U.S. Pat. Nos. 4,559,340. The patent refers to make an antihypertension agents. There are disclosed benzothiadiazinyl and quinazolinyl substituted carboxylalkyl dipeptides, wherein the benzothiodiazinyl oror quinazolinyl portions are joined to the dipeptide portions by an aminocarbonyl group. Compounds of this patent are used for the treatment of congestive heart failure and glaucoma. In addition, compounds of this patent also have diuretic activity. Web site: http://www.delphion.com/details?pn=US06428822__
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Fatty analogues for the treatment of obesity, hypertension and fatty liver Inventor(s): Berge; Rolf (B.o slashed.nes, NO) Assignee(s): Thia Medica AS (Bergen, NO) Patent Number: 6,441,036 Date filed: January 27, 2001 Abstract: The present invention relates to novel fatty acid analogous of the general forumla I: CH.sub.3 --[CH.sub.2 ].sub.m --[x.sub.i --CH.sub.2 ].sub.n --COOR, as defined in the specification, which can be used for the treatment and/or prevention of obesity, fatty liver and hypertension. Further, the invention relates to a nutritional composition
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comprising such fatty acid analogues, and a method for reducing the total weight, or the amount of adipose tissue in an animal. The invention also relates to a method for improving the quality of product such as meat, milk and eggs. Excerpt(s): The present invention relates to novel fatty acid analogous which can be used for the treatment and/or prevention of obesity, fatty liver and hypertension. Further, the invention relates to a nutritional composition comprising such fatty acid analogues, and a method for reducing the total weight, or the amount of adipose tissue in an animal. The invention also relates to a method for improving the quality of product such as meat, milk and eggs... Hyperlipidemia and obesity afflict an increasing proportion of the population in Western societies and are associated with the development of serious conditions such as atherosclerosis, hypertension, fatty liver and insulin resistance. These conditions may eventually lead to the clinical manifestations of coronary heart diseases (CD) and non-insulin dependent diabetes mellitus (NIDDM)... Treatment with modified fatty acids represent a new way to treat these diseases. Web site: http://www.delphion.com/details?pn=US06441036__ •
Genes and proteins predictive and therapeutic for stroke, hypertension, diabetes and obesity Inventor(s): Shimkets; Richard A. (West Haven, CT) Assignee(s): CuraGen Corporation (New Haven, CT) Patent Number: 6,486,299 Date filed: September 28, 1998 Abstract: Common human diseases like diabetes and hypertension have been demonstrated to possess an associated genetic component composed of numerous underlying genetic defects. Traditional positional cloning of genes which possess the mutations responsible for complex disease has been hindered by both the low statistical power each locus may afford, and by the technically-laborious nature of the positional cloning methodologies. Disclosed herein is a methodology for the rapid identification of the genes responsible for quantitative trait loci (QTL) comprised of comprehensive gene expression analysis in organs relevant to disease in combination with the positional mapping of known QTL, so as to quantitatively identify candidate genes. This aforementioned methodology was applied to a total of five tissues/organs derived from the spontaneously hypertensive rat (SHR), the stroke-prone variant of the SHR (SHR-SP) and control Wistar Kyoto rats (WKY). Collectively these animals vary genetically in their predisposition to stroke, insulin sensitivity, blood pressure and body weight. These traits segregate into more than a dozen identified. The present invention discloses the differential-expression of sixty genes by GeneCalling.RTM. within five different tissues/organs among these animals. Additionally, five of the sixty genes were demonstrated to be localized within chromosomal regions linked to these traits of interest and possess amino acid substitutions which may contribute to the phenotype. Excerpt(s): The present invention discloses a set of genes which have been demonstrated to be anomalously regulated (i.e., dysregulated) in a model of combining a pathophysiological predisposition towards stroke, hypertension, diabetes and obesity. The present invention also relates to methods of treating and/or preventing stroke, hypertension, diabetes or obesity by the administration of the nucleic acids or protein products (and derivative and analogs thereof) of the GENE SET which are defective and/or are of low abundance in humans. The present invention further relates to
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methodologies of diagnosis, prognosis and screening for alleles of the GENE SET which may cause or predispose to the aforementioned diseases... Prevalent human diseases such as hypertension, non-insulin dependent diabetes (NIDDM), stroke, and obesity (dyslipidemia) have been shown to possess a significant genetic component composed of multiple, perhaps numerous, underlying genetic defects. Human Metabolic Syndrome X, a relatively common but poorly understood disorder, has been shown to possess a significant genetic component which is comprise of an association of the pathophysiologies of hypertension, insulin resistance, dyslipidemia and abdominal obesity. See e.g., Ferrannini, et al., 1987. New Engl. J. Med. 317:350-357; Kaplan, 1989. Arteriosclerosis 9:335-344. Given the prevalence of this combination of diseases, many research groups have focussed their efforts upon determining the etiology (i.e., the primary causative genetic defects) of Metabolic Syndrome X in humans and closelyassociated animal models... The most successfully studied of these aforementioned diseases to date is hypertension, with strong evidence nucleotide sequence variants, with their associated amino acid residue substitutions, within a total of 11 human genes affect blood pressure. See e.g., Shimkets, et al., 1994. Cell 79(3):407-414; Simon, et al., 1997. Nat. Genet. 17(2):171-178; Geller, et al., 1998. Nat. Genet. 19(3):279-281. While in all probability these variants, in toto, account for only a fraction of the variation in blood pressure within the general population, they, nonetheless, serve to illustrate the potential that the etiology of many such diseases may involve the interaction of a large number of genetic components. As the majority of the genetic components of complex diseases such as human Metabolic Syndrome X have yet to be elucidated, a comprehensive analysis for the genetic defects responsible for the phenotype was undertaken in the present invention within a closely-associated animal model of this syndrome. Web site: http://www.delphion.com/details?pn=US06486299__ •
Herbal compositions and their use as agents for control of hypertension, hypercholesterolemia and hyperlipidemia Inventor(s): Borah; Kripanath (Morris Plains, NJ), Tomer; Onkar S. (Watchung, NJ), Glomski; Peter (South Amboy, NJ) Assignee(s): Chromak Research, Inc. (Bound Brook, NJ) Patent Number: 6,162,438 Date filed: June 24, 1999 Abstract: Edible herbal compositions for use as agents for the control of hypertension, hypercholesterolemia and hyperlipidemia in mammals. The edible composition is a mixture of at least three, preferably at least six, herbs selected from the group consisting of Terminalia arjuna, Cynara scolymus, Zingibar officinale, Allium sativum, Crataegus oxycantha, Curcuma longa, Boerhaavia diffusa and Trigonella foenumgraecum. The composition preferably contains the herbs in approximately equal amounts. Excerpt(s): The present invention is directed to edible herbal compositions for use as agents for control of hypertension, hypercholesterolemia and hyperlipidemia in mammals. The composition comprises a synergistic mixture of at least three herbs selected from a group of eight herbs identified below... The prior art is replete with references to herbal medicines for treatment of a variety of ailments in mammals. Typically, such herbal medicines are obtained as the active compound(s) by extraction from plant tissues. Although the use of various herbs have been described in related areas, the synergistic combination of the edible herbs for use as agents for control of
Patents 277
hypertension, hypercholesterolemia and hyperlipidemia in mammals has never previously been described... There currently exists a great need for non-synthetic, holistic therapeutic compositions for the control of hypertension (i.e. high blood pressure), hypercholesterolemia (high cholesterol levels) and hyperlipidemia (high triglyceride levels) in mammals. It has been found that the herbal compositions of the invention are synergistic in their effect and daily ingestion of such compositions of the invention is an effective therapeutic method of achieving such control without the troublesome side effects on the liver, digestive system and kidneys associated with synthetic drugs. Web site: http://www.delphion.com/details?pn=US06162438__ •
Hypertension analyzer apparatus Inventor(s): DeMarzo; Arthur P. (2S558 White Birch La., Wheaton, IL 60187) Assignee(s): none reported Patent Number: 5,031,629 Date filed: June 2, 1989 Abstract: The present invention is directed to an apparatus that is compact, portable and highly effective in performing a hemodynamic profile of a patient, and is particularly useful in generating such profiles for the purpose of diagnosing and treating hypertension. The apparatus includes noninvasive blood pressure and cardiac output monitors, computing means and the apparatus calculates a patient's cardiac index and systemic vascular resistance index for use in diagnosing hypertension. Excerpt(s): The present invention generally relates to apparatus for performing hemodynamic analysis on patients, and more specifically relates to a self-contained, compact, noninvasive apparatus for performing such hemodynamic analysis... While much research is being conducted on hypertension, particularly with respect to the causation and treatment of the condition, it is generally believed that hypertension is caused by an increase in cardiac output of the patient or by a gradual increase in the systemic vascular resistance of the patient. The hemodynamic characteristics of a patient's system can be defined by the relationship between the systemic vascular resistance, the mean arterial pressure, and the cardiac output. It is generally known that the brain controls the arterial pressure in providing adequate perfusion of a patient, and increases the pressure if an increased systemic vascular resistance condition exists... The most common diagnosis of hypertension through noninvasive procedures involves the measurement of systolic and diastolic arterial pressures and a comparison of those measured values with what are considered to be normal for patients of the same sex, age and known conditions. Web site: http://www.delphion.com/details?pn=US05031629__
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Hypertension-treatment and cholesterol-depressant composition comprising extract from mixture of Panax notoginseng and Salvia miltiorrhiza and method of preparing the same Inventor(s): Hong; Eun Kyung (Seoul, KR), Chung; Young Shin (Seoul, KR) Assignee(s): Medvill Co., Ltd. (Seoul, KR) Patent Number: 6,589,572 Date filed: June 14, 2001 Abstract: A composition for treating hypertension and lowering cholesterol is provided which contains the mixed extract of Panax notoginseng and Salvia miltiorrhiza as an active ingredient thus lowering and maintaining blood pressure substantially constant. Also provided is a method for preparing composition containing the mixed extract of Panax notoginseng and Salvia miltiorrhiza as an active ingredient. Excerpt(s): The present invention relates to a composition for treating hypertension and lowering cholesterol and a method for preparing same. More specifically, the present invention relates to a composition for treating hypertension and lowering cholesterol which contains the mixed extract of Pana notoginseng and Salvia miltiorrhiza as an active ingredient, and a method for preparing same... Cardiac and vascular diseases are one of the main causes of human death, and are represented by cerebral hemorrhage, cerebral thrombosis, heart failure, cardiac infarction, etc. However, etiology of such diseases is very diverse and complex. The target for treatment of hypertension is to prevent the occurrence of complications in brain, heart, kidney, liver, etc., thereby allowing the human to manage a normal life by the average life span. The development of drugs for treatment of hypertension is still urgently required... Blood pressure and hypertension will be more specifically explained hereinbelow. The term, blood pressure, denotes a pressure of blood stream flowing through blood vessels, i.e., arterial pressure. In this context, the term, hypertension, means that a certain cause induces an increase of resistance on the internal wall of blood vessel thus resulting in the maximum blood pressure (systolic blood pressure or highest blood pressure) of 150-160 mmHg and the minimum blood pressure (diastolic blood pressure or lowest blood pressure) of 90 mmHg or more. The former is called a systolic hypertension and the latter is called a diastolic hypertension. Although both may separately arise, it is general that they are simultaneously present. Moreover, hypertension may occur in the thirties, but it mainly occurs during the pre- and post-climacteric period in men rather than women. Web site: http://www.delphion.com/details?pn=US06589572__
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In ovo use of L-arginine and salts thereof in the prevention and/or treatment of pulmonary hypertension syndrome in avians Inventor(s): Bottje; Walter G. (Fayetteville, AR), Wideman, Jr.; Robert F. (Fayetteville, AR) Assignee(s): The Board of Trustees of the University of Arkansas (Little Rock, AK) Patent Number: 6,127,421 Date filed: January 31, 1997 Abstract: A method of treating an avian egg, including the step of administering to an avian egg a sufficient amount of an L-arginine compound to prevent pulmonary hypertension syndrome in an avian to be hatched from the egg.
Patents 279
Excerpt(s): The present invention relates to treatment of avians. In another aspect, the present invention relates to the use of L-arginine for the treatment of avians. In even another aspect, the present invention relates to the administration of L-arginine to avians in ovo for the treatment of or prevention of pulmonary hypertension syndrome, also commonly known as ascites in poultry... Pulmonary hypertension syndrome was reported as early as 1968, and is a condition characterized by mortality with the accumulation of fluid (ascites fluid) in the abdomen of the bird. Ascites fluid accumulation in the body cavity may also be caused by tumor growth in the abdominal cavity. Pulmonary hypertension syndrome is caused by a high resistance to blood flow through the lungs. This excessive resistance of blood flow through the lungs causes an adverse effect on the heart, and hence pulmonary hypertension syndrome. As used hereinafter, "ascites" and "pulmonary hypertension syndrome" will be used interchangeably with the understanding that this form of ascites in poultry is in no way related to tumor growth... Pulmonary hypertension syndrome poses a serious problem to young fast growing poultry all over the world. First associated with flocks raised at high altitude, it is now recognized that other factors, such as cold temperatures, rapid growth, respiratory distress, high salt intake, and poor ventilation, also encourage pulmonary hypertension syndrome. Death from pulmonary hypertension syndrome results due to an enlarged heart, specifically including dilation and hypertrophy of the right ventricle. Congestive heart failure develops leading to liver damage, and kidney lung and intestinal problems, and compression of the air sac with abdominal fluids. While traditionally, male birds were at greater risk than females because of their faster growth rate, the conditions of modern poultry farming have caused female birds to suffer almost equally. Web site: http://www.delphion.com/details?pn=US06127421__ •
Inhalational treatment of pulmonary hypertension and related conditions Inventor(s): Buckle; Derek R. (Epsom, GB2), Williams; Andrew J. (Epsom, GB2) Assignee(s): Beecham Group p.l.c. (Brentford, GB2) Patent Number: 5,554,610 Date filed: August 24, 1994 Abstract: A method for the treatment and/or prophylaxis of disorders associated with pulmonary hypertension and/or disorders associated with right heart failure, in mammals, such as humans, which method comprises administering to the mammal in need of such treatment and/or prophylaxis an effective and/or prophylactic amount of a vasodilator selected from the group consisting of ganglion blockers, sympathetic nerve blockers, and direct vasodilators; or a pharmaceutically acceptable salt thereof or a pharmaceutically acceptable solvate thereof. Excerpt(s): The present invention relates to a method for the treatment and/or prophylaxis of disorders associated with pulmonary hypertension... United Kingdom Patent No. 1489879 discloses the compound N"-Cyano- N-4-pyridyl-N'-1,2,2trimethylpropylguanidine and, in Example 47, a process by which it can be prepared. The compound, which is referred to herein by its common name, pinacidil, is described in the patent as a hypotensive compound. In "Drugs of the Future" Vol. VI(3), 149, 1981, pinacidil is described as a vasodilator... It has now been discovered that pinacidil is of potential use in the treatment of disorders associated with pulmonary hypertension and/or of disorders associated with right heart failure, particularly when administered by inhalation. It is also believed that the administration by inhalation of any such
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vasodilator will be of potential use in the treatment of disorders associated with pulmonary hypertension and/or of disorders associated with right heart failure. Web site: http://www.delphion.com/details?pn=US05554610__ •
Materials and methods for the treatment of hypertension and angina Inventor(s): Milner; Peter G. (Los Altos Hills, CA), Zhang; Xiaoming (Campbell, CA), Pfister; Jurg (Los Altos, CA), Druzgala; Pascal (Santa Rosa, CA) Assignee(s): ARYx Therapeutics (Santa Clara, CA) Patent Number: 6,608,097 Date filed: October 10, 2002 Abstract: The subject invention provides useful and novel calcium channel blockers based upon mibefradil. The subject invention also provides methods for synthesizing the compounds of the invention. The invention also provides methods for the control or prevention of hypertension, angina pectoris, ischemia, arrhythmias, and cardiac insufficiency in a patient by administering a compound, or composition, of the invention to an individual in need of such treatment. Excerpt(s): Adverse drug-drug interactions (DDI), elevation of liver function test (LFT) values, and QT prolongation leading to torsades de pointes (TDP) are three major reasons why drug candidates fail to obtain FDA approval. All these causes are, to some extent metabolism-based... Oxidative metabolism is the primary metabolic pathway by which most drugs (xenobiotics) are eliminated. It is also the major source of drug toxicity, either intrinsic toxicity or toxicity due to drug-drug interactions (DDI). Adverse DDI as well as intrinsic toxicity due to metabolites are a major reason for the failure of drug candidates in late-stage clinical trials. Many DDI are metabolism based, i.e., two or more drugs compete for the same metabolizing enzyme in the cytochrome P450 system (CYP450) [Guengerich, F. P. (1997) Role of cytochrome P450 enzymes in drug-drug interactions. In: Drug-drug interactions: scientific and regulatory perspectives. Li, A P (ed.)Academic Press, San Diego pp7-35 and Shen, W. W. (1995) Int. J. Psychiatry Med. 25:277-290]. Non-oxidative metabolic systems, such as hydrolytic enzymes, on the other hand, do not depend on co-factors; are not inducible; have a high substrate capacity; do not have a high degree of inter-individual variations in man; and are present in most tissues and organs. Non-oxidative metabolic systems are, therefore, much more reliable... Metabolism-based DDI take place when two (2) or more drugs compete for metabolism by the same enzyme. These metabolic interactions become relevant to DDI when the metabolic system is inducible or/and easily saturable. Such metabolic interactions lead to modification of the pharmacokinetics of the drugs and potential toxicity. Web site: http://www.delphion.com/details?pn=US06608097__
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Medication indicated for ocular hypertension Inventor(s): Shell; John W. (Hillsborough, CA), Gale; Robert M. (Mountain View, CA) Assignee(s): ALZA Corporation (Palo Alto, CA) Patent Number: 4,303,637 Date filed: April 4, 1980
Patents 281
Abstract: An ocular therapeutic system is disclosed for dispensing a medicament to an ocular environment. The system comprises a beta-blocking drug in a polymer with the drug surrounded by the polymer. A method is disclosed for the management of ocular hypertension using the system. Also disclosed, is a composition comprising the drug and the polymer. Excerpt(s): This invention relates to ocular pharmacology. More particularly, the invention pertains to (1) a noval and useful ocular therapeutic system housing a betaadrenergic blocking osmotically effective solute, and to (2) a method for the management of intraocular pressure by dispensing the drug solute from the system to an eye. Also, the invention concerns a composition of matter comprising the solute and the polymer, which composition is useful for manufacturing a dispensing system... Recently, a beta-blocking drug, timolol, was introduced to ocular pharmacology in solution form as an useful drug for the management of intraocular pressure. This drug is administered to the eye as liquid eyedrops for lowering intraocular pressure associated with glaucoma, as described by Zimmerman et al, in Invest. Ophthalmol. Visual Sci., Vol. 16, pages 623 to 624, 1977; and by Wettrell et al, in Brit. J. of Ophthal., Vol 61, pages 334 to 338, 1977... While, the eyedrop method of administration is suitable in a few instances, serious limitations are associated with its use. For example, eyedrops exhibit a relatively brief residence time in the eye, necessitating frequent reapplication, usually 1 to 4 times daily, and sometimes more frequently. Another limitation of the eyedrop is volumetric. The normal volume to which the ocular tear film can increase is limited before it overflows, and the action of eye-blinking reduces this volume; yet, the conventional dropper delivers drops that exceed this volume. Thus, the familiar act of instilling eyedrops is complicated, as the reflux blinking that accompanies this act results in a loss of administered drug from the tear film, and consequent removal of drug from contact with the eye. These limitations impose an uncertainty on the quantity of drug delivered and they force the therapist to seek an improved form of therapy; see Wright et al., Arch. Ophthalmol., Vol. 67, pages 564 to 565, 1962; and Mishima et al., Ophthalmol., Vol. 5, pages 264 to 276, 1966. Web site: http://www.delphion.com/details?pn=US04303637__ •
Method and apparatus for monitoring and diagnosing hypertension and congestive heart failure Inventor(s): Cohn; Jay N. (Minneapolis, MN), Finkelstein; Stanley M. (St. Louis Park, MN) Assignee(s): Regents of the University of Minnesota (Minneapolis, MN) Patent Number: 4,899,758 Date filed: August 2, 1988 Abstract: Apparatus and method for monitoring and diagnosing CHF and hypertension includes digitizing brachial artery pulses and determining C.sub.2 from modified Windkessel model. CHF and hypertension are monitored and diagnosed by tracking C.sub.2 values and testing values against a disease discriminating threshold of 0.08 ml/mm Hg. Excerpt(s): The present invention pertains generally to cardiac medicine and more particularly to the diagnosis and monitoring of congestive heart failure (CHF) and hypertension in humans... The characteristics of the peripheral vasculature are important in determining arterial pressure and left ventricular performance in patients
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with congestive heart failure (CHF) and hypertension. Peripheral vascular resistance is the parameter most frequently used to describe the peripheral vascular bed. However, recent studies suggest that frequency-dependent vascular impedance may be a more sensitive indicator of disease and therapeutic response. The determination of this impedance requires Fourier analysis of simultaneously recorded pressure and blood flow waveforms. Heretofore, pressure and waveforms have typically been measured at the ascending aorta, requiring significant system invasion, and thus limiting the usefulness of the procedure as a diagnostic and monitoring tool... An alternative impedance measurement technique uses the peripheral arterial pressure pulse contour and a measure of cardiac output to derive vascular impedance properties. This method is minimally invasive, requiring only a brachial artery puncture to obtain the peripheral pressure signal, and thus offers the potential of practical clinical use. Proximal compliance, distal compliance, inertance and peripheral resistance are all determinable from the pressure pulse contour and cardiac output. As set forth below, the present invention utilizes the alternative impedance measuring technique to diagnose and monitor the vascular abnormalities and characteristics of hypertension and CHF. Web site: http://www.delphion.com/details?pn=US04899758__ •
Method and ophthalmic composition for treating ocular hypertension and glaucoma with butyrophenones Inventor(s): Chiou; George C. Y. (College Station, TX) Assignee(s): The Texas A&M University System (College Station, TX) Patent Number: 4,565,821 Date filed: March 21, 1983 Abstract: Aqueous humor formation and intraocular pressure in mammals having ocular hypertension or glaucoma may be reduced by topically administering to a hypertensive eye an ophthalmologically acceptable amount of a dopamine antagonist or acid addition salt thereof. A preferred group of dopamine antagonists is the butyrophenones, especially haloperidol, trifluperidol, and moperone. An ophthalmic composition for topically treating glaucoma may comprise an aqueous solution containing 0.01% to 5% by weight of a water-soluble ophthalmologically acceptable acid addition salt of such dopamine antagonist. Excerpt(s): This invention relates to ophthalmologically acceptable dopamine antagonists and ophthalmologically acceptable acid addition salts thereof and their use to lower intraocular pressure, especially in the treatment of ocular hypertension and glaucoma... Glaucoma is an optical neuropathy associated with elevated intraocular pressures which are too high for normal function and result in irreversible loss of visual function. If untreated, glaucoma may eventually lead to blindness. Ocular hypertension, i.e., the condition of elevated intraocular pressure without optic nerve head damage or characteristic glaucomatous visual field defects, is now believed by many ophthalmologists to represent the earliest phase of glaucoma... Many of the drugs formerly used to treat glaucoma proved not entirely satisfactory. Indeed, few advances have been made in the treatment of glaucoma since pilocarpine and timolol were introduced. Timolol, 1-tert-butylamino -3-[(4-morpholino-1,2,5-thiadiazol-3-yl) oxy]-2propanol, is a, .beta.-adrenergic blocking agent which has been found to be effective in reducing intraocular pressure without many of the undesirable side effects associated with pilocarpine. In addition, timolol possesses advantages over many other .beta.adrenergic blocking agents, including a lack of local anesthetic action, long duration of
Patents 283
activity, and minimal tolerance. Nevertheless, timolol must be used with caution in those patients having elevated intraocular pressure who also suffer from bronchial asthma, sinus bradycardia with greater than first degree block, cardiogenic shock, right ventricular failure secondary to pulmonary hypertension, or congestive heart failure. Further, the concomitant use of timolol with adrenergic augmenting cyclopropane-like drugs must be carefully monitored. These precautions are necessary because even when administered topically to the eye, timolol is sufficiently active that a small portion is absorbed into the systemic circulation where it can affect other systems. Web site: http://www.delphion.com/details?pn=US04565821__ •
Method for controlling hypertension Inventor(s): Ho; Winston (Hatfield, PA), Mohrbacher; Richard (Maple Glen, PA), Tutwiler; Gene (Churchville, PA) Assignee(s): McNeilab, Inc. (Fort Washington, PA) Patent Number: 4,370,343 Date filed: September 21, 1981 Abstract: Hypertension is controlled by administration of glycidic or thioglycidic acid derivatives substituted in the .alpha.-position with a long chain alkyl or alkenyl or dibromoalkyl radical. Excerpt(s): This invention relates to a method for controlling hypertension in hypertensive animal subjects by administering a therapeutically effective antihypertensive amount of a glycidic or thioglycidic acid derivative which is substituted in the .alpha.-position with a long chain alkyl or alkenyl or dibromoalkyl radical... As used herein, the term "loweralkyl" refers to straight or branch chained saturated hydrocarbons having from 1 to 5 carbons, e.g., methyl, ethyl, propyl, isopropyl, sec-butyl, pentyl and the like alkyls... The preferred compounds, for use in the antihypertensive method of the present invention are those of Formula (I) wherein R is a long chain alkyl, CH.sub.3 --(CH.sub.2).sub.n, wherein n is an integer from 7 to 19, and wherein R.sub.1 and R.sub.2 are each hydrogen. Web site: http://www.delphion.com/details?pn=US04370343__
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Method for controlling hypertension and compositions Inventor(s): Rasmussen; Chris R. (Ambler, PA) Assignee(s): McNeilab, Inc. (Fort Washington, PA) Patent Number: 4,229,462 Date filed: December 22, 1978 Abstract: A method for controlling hypertension by administering to hypertensive subjects a N-aryl-N'-(2-imidazolidinylidene)urea compound and compositions suitable therefor are described. Excerpt(s): This invention relates to method for controlling hypertension employing Naryl-N'-(2-imidazolidinylidene)urea compositions... Certain imidazolidine ureas are known in the art. Thus, in U.S. Pat. No. 3,168,520 imidazolidine ureas and hexahydropyrimidine ureas are taught. These compounds are taught to be useful as dye
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stabilizers. The patent specifically teaches 2-phenylcarbiliminoimidazolidine which is N(2-imidazolidinylidene)-N'-phenylurea. There is no teaching or suggestion in the patent however for the use of imidazolidineureas and hexahydropyrimidineureas as active ingredients in pharmaceutical compositions... Some urea compounds have been disclosed to have certain pharmacological properties. Thus, U.S. Pat. No. 4,060,635 discloses amidinoureas. These compounds have an aryl group on one urea nitrogen and a substituted amidino group on the other urea nitrogen. U.S. Pat. Nos. 3,539,616 and 3,784,582 teach amidinoureas in which one urea nitrogen is substituted with an aryl group and the other urea nitrogen is substituted with an unsubstituted amidino group. U.S. Pat. No. 4,058,557, also directed to amidinoureas but more remote, teaches compounds in which one of the amidino nitrogens necessarily is attached to an oxygen. None of the patents teach or suggest the substitution of an imidazolidino group on a urea nitrogen. None of these patents teach or suggest anti-hypertensive activity. Web site: http://www.delphion.com/details?pn=US04229462__ •
Method for detecting a marker for essential hypertension and diagnostic use thereof Inventor(s): Abbott; Richard E. (Englewood, NJ), Cowen; Lisa A. (New York, NY), Kowarski; Szloma (Bronx, NY), Schachter; David (Bronx, NY) Assignee(s): The Trustees of Columbia University in the City of New York (New York, NY) Patent Number: 4,840,894 Date filed: March 4, 1986 Abstract: A method for detecting the presence in a human of an integral membrane calcium-binding protein associated with essential hypertension which comprises isolating tissue from a human, treating the tissue to obtain integral membrane proteins, contacting the proteins thus obtained with a first antibody molecule which binds to the integral membrane calcium binding protein to form an detectable protein-antibody complex, and detecting the complex so formed.Further, methods for quantitatively determining the amount of an integral membrane calcium-binding protein and the messenger RNA encoding said protein, diagnostic methods for identifying individuals predisposed to essential hypertension, and protein and messenger RNA associated with said hypertension. Excerpt(s): Throughout this application various publications are referenced by a number within parentheses. Full citations for these publications may be found at the end of the specification immediately preceding the claims. The disclosures of these publications in their entireties are hereby incorporated by reference into this application in order to more fully describe the state of the art to which this invention pertains... Arterial hypertension is a condition of sustained elevated systemic arterial blood pressure. The minimum level of systemic arterial pressure considered to be hypertensive has been arbitrarily set at 140/90 mm Hg. While hypertension usually involves elevations in mean and pulse pressures, the rise in diastolic pressure is clinically regarded as the critical criterion, suggesting that hypertension is due primarily to an increased peripheral resistance... Hypertension is a serious cardiovascular disease. It is responsible for approximately 10 percent of deaths in people over 50 years of age. However, many of the people in this group may have blood pressures as high as 170/90 without displaying any symptoms of hypertension, and approximately 75 percent of these individuals die of diseases which may have caused their hypertension.
Patents 285
Web site: http://www.delphion.com/details?pn=US04840894__ •
Method for detecting bacteria in urine and for treating rheumatoid arthritis, essential hypertension and other diseases associated with bacteriuria Inventor(s): Hyman; Edward S. (3420 Jefferson Ave., New Orleans, LA 70125) Assignee(s): none reported Patent Number: 4,673,637 Date filed: April 23, 1984 Abstract: A novel method of urine specimen preparation comprising intense centrifugation and a lipid wash mitigates or prevents loss of bacteria-containing sediment prior to examination. Modifications of the method facilitate examination of urines with interfering constituents such as glucose, phosphates, and soluble and insoluble proteins. By this method, bacteria have been found in the urine of patients suffering from rheumatoid arthritis and essential hypertension. These bacteria were not detected in standard urine preparations. Administration of antibiotic agents effective against the bacteria detected, such as clindamycin, destroyed these bacteria and provided therapeutic relief. Excerpt(s): This invention relates to a new method of detecting abnormal levels of bacteria in urine, and to new methods for the treatment of patients suffering from rheumatoid arthritis, essential hypertension, and other diseases in which significant bacteriuria was detected by the novel specimen preparation of the present invention that would not have been easily demonstrated by known procedures... The direct microscopy and the culture methods each have pitfalls In the past 20-25 years the direct visualization of bacteria in urine has largely been abandoned in favor of the methods involving culturing and counting the colonies of bacteria. Indeed virtually all of the studies of the significance of bacteriuria are based upon culturing the urine, and the direct microscopic examination of urine has been relegated to the status of a quick but inadequate screening procedure which may be helpful because it can be correlated with the culture methods... Rheumatoid arthritis (RA) is a chronic inflammation of the joints, generally regarded as a systemic autoimmune disorder. Its etiology is unknown, but it has been postulated that it is associated with microbial infection. See, e.g., D. C. Demonde, ed., Infection and Immunity in the Rheumatic Diseases, 95-287 (Blackwell Scientific Publications, London: 1976). The evidence, however, until the present discovery, was inconclusive. See, e.g., D. J. McCarty, et al., ed., Arthritis and Allied Conditions: A Textbook of Rheumatology, ch 28 at 417 (9th ed. 1979); R. G. Petersdorf, et al., ed., Harrison's Principles of Internal Medicine, Part Six, Chapter 346, at 1977 (McGraw Hill: 1983). Bacteriuria has not been associated with RA, and indeed one authority remarks "Urinary abnormalities are relatively uncommon in RA . Urinary tract infection was not found to be increased in RA patients." McCarty, supra, chapter 33, page 499, citing Ann. Rheum. Dis., 27: 345 (1968). Hypertension is a chronic elevation of blood pressure resulting from the obstruction of blood flow within the kidney (secondary hypertension) or without apparent cause (essential hypertension). One kidney disorder associated with secondary hypertension is pyelonephritis, the inflammation of the renal pelvis of the kidney as a result of bacterial infection, usually responsive to antibiotics. It has not been reported, however, that there is any correlation between essential hypertension and asymptomatic bacteriuria (bacteriuria observed in patients not reporting symptoms of urinary tract disorders). According to N. M. Kaplan, Clinical Hypertension, 14 (3d. ed. 1982), bacteriuria is found in 2-5% of hypertensives.
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Most of these positive cultures were of gram-negative rods. The method of the present invention has demonstrated a much higher incidence of bacteriuria in hypertensives, perhaps as high as 90%, and that cocci or "exploded cocci" are found in considerable numbers. Web site: http://www.delphion.com/details?pn=US04673637__ •
Method for diagnosing, monitoring and treating hypertension Inventor(s): Finkelstein; Stanley M. (St. Louis Park, MN), Cohn; Jay N. (Minneapolis, MN) Assignee(s): Regents of the University of Minnesota (Minneapolis, MN) Patent Number: 5,054,493 Date filed: February 5, 1991 Abstract: A method for diagnosing, monitoring and treating hypertension uses the parameter C.sub.2 of the modified Windkessel model as an indication of the hypertensive disease condition. Apparatus for determining the parameter C.sub.2 (i.e. distal vascular compliance) of the modified Windkessel model includes means for obtaining a pressure pulse contour and a cardiac output value and for determining the model parameters. Excerpt(s): The present invention relates generally to the fields of cardiac and circulatory medicine, and more particularly to the medical disorder of hypertension... Hypertension is defined as abnormally elevated blood pressure. More specifically, when a person under conditions of rest consistently has a blood pressure that exceeds 145/90 (systole/diastole), the person is said to have high blood pressure or hypertension. It is currently believed that over fifty million people in the United States have hypertension and fifteen to twenty percent of all deaths in people over fifty years of age occur as a direct or indirect result of hypertension. Actuarial statistics show that the disability and mortality rates of hypertensive persons are higher for each age bracket than for persons with normal blood pressure. Specific ailments attributable to hypertension include heart failure, myocardial infarction, rupture or thrombus of the blood vessels in the brain and kidney damage... Despite the prevalence of hypertension and its potentially severe consequences to health, its detection, treatment and diagnosis remains entirely dependent on blood pressure measurements. However, the presence of high blood pressure in a patient at any given time only establishes that the patient's blood pressure at that moment is high; it says nothing about the patient's underlying medical condition. Substantial transient variations in blood pressure, for example as caused by digestion, exercise, posture, circadian rhythms and emotional states, occur on a regular basis in any individual. Thus, it is not possible to tell, absent continuous measurements and periodic followup over time, whether a hypertensive state is a function of a transient condition or is of a chronic nature. Blood pressure measurements in and of themselves do not reveal the presence of the hypertensive disease condition, which can be defined as the process or presence of underlying physical changes in the human body which result in the state of hypertension. Web site: http://www.delphion.com/details?pn=US05054493__
Patents 287
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Method for diagnosing, monitoring and treating hypertension and other cardiac problems Inventor(s): Chio; Shiu-Shin (Rancho Santa Fe, CA) Assignee(s): Pulse Metric, Inc (San Diego, CA) Patent Number: 6,540,687 Date filed: December 15, 2000 Abstract: A method is disclosed for diagnosing, monitoring and treating cardiovascular pathologies. Among the hemodynamic parameters of interest are peripheral resistance, compliance, and cardiac (left ventricular) output. Peripheral resistance determined according to the present invention has been found to be a reliable indicator, not only of hypertension, but also of the cause of the hypertension. The determined peripheral resistance can be compared against a predetermined threshold value. This comparison helps to foster a diagnosis of a hypertensive condition. Excerpt(s): The present invention relates to a method for diagnosing, monitoring and treating cardiovascular pathologies, and more particularly to a method of determining hemodynamic parameters in a human cardiovascular system by analyzing arterial waveforms, methods for using the parameters so determined for diagnosing hypertension and other cardiovascular problems and diseases, and devices that incorporate the methods of the present invention... Cardiovascular disease is a leading cause of death and disability. One cardiovascular disease that affects a large number of people is hypertension, which is defined as abnormally elevated blood pressure. Hypertension is quite common. It is estimated that over 60,000,000 Americans suffer from hypertension... To prevent cardiac disorders from causing death, serious illness and disability, it is important to monitor the condition of a person's cardiovascular system, and to analyze the data from the monitoring so performed to determine whether any pathologies exist in the person's cardiovascular system that should be treated to prevent further degradation of the patient's cardiovascular system. Web site: http://www.delphion.com/details?pn=US06540687__
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Method for preventing onset of hypertension employing a cholesterol lowering drug Inventor(s): Tschollar; Werner (Lawrenceville, NJ), Kawano; James C. (Narberth, PA), Yonce; Cary S. (Newtown, PA), Bergey; James L. (Lansdale, PA) Assignee(s): E. R. Squibb & Sons, Inc. (Princeton, NJ) Patent Number: 5,593,971 Date filed: May 22, 1995 Abstract: A method is provided for preventing or reducing the risk of hypertension in normotensive patients having insulin resistance by administering a cholesterol lowering drug, such as pravastatin, alone or in combination with an ACE inhibitor, especially one containing a mercapto moiety, such as captopril or zofenopril. Excerpt(s): The present invention relates to a method for preventing onset of hypertension in a normotensive mammalian species with insulin resistance by administering a cholesterol-lowering drug, preferably, an HMG CoA reductase inhibitor, such as pravastatin alone or in combination with an ACE inhibitor, such as captopril or ceranapril... The role of insulin resistance and consecutive hyperinsulinemia in the pathogenesis of non-insulin dependent diabetes (NIDDM) and atherosclerosis is
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firmly established, Olefsky, J. M., et al, "Insulin Action and Resistance in obesity and non-insulin dependent type II diabetes mellitus," Am. J. Physiol. 1982; 243:E15-E30. Reaven, G. M., "Role of insulin resistance in human disease," Diabetes 1988; 37:15951607. Stout, R. W., "Insulin and atheroma--an update," Lancet 1987; I;1077-1079. Recently the atherogenic risk of elevated insulin concentrations in prediabetic insulin resistant states like obesity, glucose intolerance, essential hypertension and--surprisingly--in "healthy" subjects with normal oral glucose tolerance has gained increasing interest, Ferrannini, E., et al, "Insulin resistance in essential hypertension," N. Engl. J. Med. 1987; 317:350-357. Standl, E., "Hyperinsulinamie--eine Ursache der Makroangiopathie?" Akt Endokr Stoffw 1989; 10:41-46 (Sonderheft). Stout, R. W., supra, Torlone E., et al, "Effects of captopril on insulin-mediated carbohydrate and lipid metabolism in subjects with NIDDM and hypertension, "Diabetes 1989; 38(Suppl. 2):88A. Hyperinsulinemia appears to be the earliest and strongest detectable risk factor for coronary heart disease, Eschwege, E., et al, "Coronary heart disease mortality in relation with diabetes, blood glucose and plasma insulin levels. The Paris Prospective Study, ten years later," Horm. Metab. Res. Suppl. 1985; 15:41-46. Modan, M., et al, "Hyperinsulinemia--a link between glucose intolerance, obesity, hypertension, dyslipoproteinaemia, elevated serum uric acid and internal kation imbalance," Diab. Met. 1987; 13:375-380, and as a recent prospective study showed, insulin resistant hypertensive subjects have a markedly elevated risk to develop NIDDM in addition to their already high atherogenic risk, Skarfors, E. T., et al, "Do anti-hypertensive drugs precipitate diabetes in predisposed man?" Br. Med. J. 1989; 298:1147-1152... Pollare, T., et al, "Insulin Resistance is a Characteristic of Primary Hypertension Independent of Obesity," Metabolism, Vol. 38, No. 12 (December), 1989:pp 1-9 discloses that hypertension is associated with hyperinsulinemia independently of either obesity or glucose tolerance. Web site: http://www.delphion.com/details?pn=US05593971__ •
Method for preventing or treating low renin hypertension by administering an endothelin antagonist Inventor(s): Bird; Joan Eileen (Princeton, NJ) Assignee(s): Bristol-Myers Squibb Company (Princeton, NJ) Patent Number: 5,916,907 Date filed: January 27, 1998 Abstract: Prevention or treatment of low renin hypertension by administration of an endothelin antagonist is disclosed. Excerpt(s): The present invention relates to the prevention or treatment of low renin hypertension by administering an endothelin antagonist... Hypertension has a variety of etiologies. Due at least in part to this, the success of a pharmacological agent in treating one form of hypertension does not necessarily indicate that that agent will be successful in treating another form of hypertension... One major contributor to hypertension is the "renin cascade", which culminates in the production of the potent vasoconstrictor angiotensin II. Renin is a protease which cleaves angiotensinogen to form angiotensin I, the latter which is then cleaved by a second enzyme (the angiotensin-converting enzyme or ACE) to form angiotensin II. Administration of a pharmacological agent which inhibits renin or ACE, or which antagonizes the angiotensin II end-product of the cascade ("AII antagonist"), can lower blood pressure and provide a route for the treatment of this form of hypertension ("essential hypertension") which affects a large portion of the hypertensive patient population.
Patents 289
Web site: http://www.delphion.com/details?pn=US05916907__ •
Method for prevention of hypertension Inventor(s): Wyllie; Michael G. (Canterbury, GB) Assignee(s): John Wyeth and Brother Limited (Maidenhead, GB2) Patent Number: 4,701,462 Date filed: March 31, 1986 Abstract: This invention provides a method for preventing the development of hypertension in a non-hypertension animal, including a human, having an elevated natriuretic hormone level, which comprises administering to said animal an amount of indoramin or a pharmaceutically acceptable salt thereof effective to lower the natriuretic hormone level. Excerpt(s): This invention relates to a novel method for the prevention of hypertension, more particularly to a treatment of elevated natriuretic hormone levels... In U.K. patent specification No. 1,218,570 there are described and claimed a class of indole derivatives which have various pharmacological activities, especially action on the cardiovascular system. One of these compounds, 3-[2-(benzamido-1-piperidyl)ethyl]indole, has demonstrated valuable antihypertensive properties in human beings in clinical trials. This compound has the internationally approved name: indoramin. I have now found that indoramin also possesses the ability to lower natriuretic hormone levels... Recent research has shown that high natriuretic hormone levels have a causative link with the genesis of hypertension--see for example Science Vol. 212 pps. 1255-1257. Evidence suggests that natriuretic hormone alters cellular sodium and potassium ion transport. This cation transport system involves a "pump" using energy released during the hydrolysis of adenosine triphosate by an enzyme called sodium--dependent adenosinetriphosphatase (Na.sup.+, K.sup.+ -ATPase). Natriuretic hormone apparently works by inhibiting this enzyme not only in the kidney but in a variety of other tissues including arterial smooth muscle. In this way the hormone forms a link between excessive dietary salt and high blood pressure. Accordingly, by its ability to lower natriuretic hormone levels, indoramim is indicated as treatment for the prevention of hypertension in those normotensives at risk with elevated natriuretic hormone levels. Web site: http://www.delphion.com/details?pn=US04701462__
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Method for reducing hypertension of a liver Inventor(s): Harbuck; Stanley C. (P.O. Box 1643, Salt Lake City, UT 84110) Assignee(s): none reported Patent Number: 4,501,263 Date filed: March 31, 1982 Abstract: In an organism having a vascular system, a device and method for diverting blood flow from one blood vessel to another, such as from the hepatic artery to the portal vein for reducing hypertension of the liver. The method includes the implantation of a device according to the invention by which blood is diverted. A conduit is inserted within one vessel, normally a vein, and blood diverted to the conduit from another vessel such as an artery, wherein the blood is mixed.
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Excerpt(s): This invention relates to a surgically implantable device for use in mixing blood and for treatment of conditions such as hypertension. In particular a device according to the invention may be used to reduce hypertension of a cirrhotic liver... The liver is connected to the vascular system through the hepatic artery and a portal vein on its proximal side and through a hepatic vein on its distal side. The hepatic artery and portal vein merge within the liver to provide the blood flow for the hepatic vein... Hypertension of the liver, for instance in a cirrhotic liver, or in the case of hepatitis, is a serious health problem. Although there exists a pharmacology for partially treating liver hypertension, no way exists as yet for reducing the amount of work the liver must perform and allow the liver to repair itself. Web site: http://www.delphion.com/details?pn=US04501263__ •
Method for the treatment of hypertension Inventor(s): Ohtake; Shinzaburo (Tokyo, JA), Igarashi; Toshiji (Tokorozawa, JA) Assignee(s): Eisai Co., Ltd. (Tokyo, JA) Patent Number: 4,088,778 Date filed: March 30, 1976 Abstract: Hypertension is therapeutically treated by the administration of a vitamin E derivative to a hypertensive. Excerpt(s): The present invention relates to a method for the treatment of hypertension comprising administering a therapeutically effective amount of a vitamin E derivative to a hypertensive... Hypertension is a common geriatric disease. With the recent increase of the number of the aged, the number of patients having hypertension is increasing. Accordingly, the treatment of hypertension is a very important problem, but since a great variety of factors are considered as causes of hypertension, no decisive method has been developed... As known antihypertensive agents, there can be mentioned Reserpine type drugs, Adrenergic blocking agents, Diuretic and hypotensive agents such as hydrochlorothiazide, hydralazine drugs and Dopa decarboxylase inhibitors. Each of these antihypertensive agents has various troublesome side effects, such as described below. Web site: http://www.delphion.com/details?pn=US04088778__
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Method for treating essential hypertension Inventor(s): Wilcox; Christopher S. (Great Falls, VA) Assignee(s): Georgetown University (Washington, DC) Patent Number: 6,096,759 Date filed: September 19, 1997 Abstract: This invention relates to the treatment of essential hypertension by administration of anti-hypertensive effective amounts of 4-hydroxy-2,2,6,6-tetramethyl1-piperidine-1-oxyl (tempol). Excerpt(s): This invention relates to the treatment of essential hypertension by administration of anti-hypertensive effective amounts of 4-hydroxy-2,2,6,6-tetramethyl1-piperidine-1-oxyl (TEMPOL)... Most, although not all, studies have demonstrated
Patents 291
blunted agonist-stimulated, endothelium-dependent vasorelaxation in the peripheral circulation of patients with essential hypertension. This suggests blunted release of endothelium-dependent relaxation factor (EDRF) or enhanced generation of endothelium-dependent contraction factor (EDCF). In the isolated aorta, there are impaired endothelium-dependent relaxation responses in spontaneously hypertensive rats (SHR) compared to their genetically normotensive controls. This has been attributed to an EDCF, which can inactivate nitrogen oxide (NO). The precise identity of EDCF remains unclear, but its generation and action depend on cyclooxygenase and thromboxane (Tx) A.sub.2 /prostaglandin (PG) H.sub.2 receptors and its actions can be prevented by blockade of oxygen free-radicals (O.sub.2.sup.-). O.sub.2.sup.- and NO interact to produce peroxynitrite, which effectively inactivates physiologic concentrations of NO... However, in contrast to the aorta, coronary artery endotheliumdependent vasodilation is normal in the SHR heart and there is enhanced release of NO from the perfused SHR heart and enhanced activity of constitutive endothelial cell type (ec) nitric oxide synthase (NOS) in cardiac endothelium of SHR. Thus, organs differ in their regulation of NO generation in genetic hypertension. Web site: http://www.delphion.com/details?pn=US06096759__ •
Method for treating hypertension using 3-(4-imidazolylmethylene)-carbazic and dithiocarbazic acid esters Inventor(s): Chan; Peter S. (Suffern, NY) Assignee(s): American Cyanamid Company (Stamford, CT) Patent Number: 4,696,940 Date filed: October 29, 1986 Abstract: This disclosure describes compositions of matter containing substituted 3-(4imidazolymethlene)carbazic and dithiocarbazic acid esters and the method of treating hypertension therewith. Excerpt(s): The 3-(4-imidazolylmethylene)carbazic and dithiocarbazic acid esters of the above formula are disclosed and claimed either generically or specifically in U.S. Pat. No. 4,124,766, together with methods for their preparation and disclosure as intermediates for the preparation of compounds which inhibit the enzyme cyclic-AMP phosphodiesterase... The compounds of the present invention are active hypotensive agents as established in the following test described by P. S. Chan and D. W. Poorvin, Clinical and Experimental Hypertension, l(6), 817-830 (1979)... Male, 16 week old, spontaneously hypertensive rats of the Okamoto strain, having an average mean arterial blood pressure (MABP) of 160.+-.1.5 mm of mercury, are used in this test. Normally, one to three rats are used per test compound. A rat is dosed by gavage with a test compound, suspended in 2% preboiled starch, at a concentration of 50 mg/ml, at the indicated dose, with 0.9% sodium chloride loading at a dose of 25 ml/kg of body weight. A second identical dose of the test compound, without sodium chloride loading, is given 24 hours later. At 28 hours after the initial dose, the mean arterial blood pressure is measured. The procedure is repeated in a second and third rat when necessary. Web site: http://www.delphion.com/details?pn=US04696940__
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Method for treating hypertension with methylreserpate Inventor(s): Katagihara; Hiroshi (Misato, JP), Fujimoto; Yasuo (Tokyo, JP) Assignee(s): Nippon Chemiphar Co., Ltd. (Tokyo, JP) Patent Number: 4,238,491 Date filed: May 9, 1978 Abstract: Hypertension in human is treated by orally administering an effective amount of methylreserpate with little or no undesirable side effect such as central nervous system depression. Methylreserpate can be prepared from Reserpine, a Rauwolfia alkaloid. Excerpt(s): The invention also relates to a pharmaceutical composition for treating hypertension in human. The composition comprises the above mentioned methylreserpate as the active ingredient and any other additive or excipient for oral administration... Hypertension, along with cancer and heart disease, is one of the typical adult diseases and, as the number of aged persons increases so does the number of hypertensitive patients. Though therapy for hypertension is a very important problem, for various reasons no decisive method of treatment has been established... Reserpine (hereinafter referred to as "RSP") and Rescinnamin (hereinafter referred to as "RCN"), which are Rauwolfia alkaloids, have long been used as remedies for hypertension because of their prolonged antihypertensive effect. However, their use is accompanied by unpleasant side effects such as uneasiness due to central nervous system depression, depressed state and loss of vitality. Thus, clinicans have been seeking RSP-type antihypertensive agents with little or no central nervous system depressive effect. Web site: http://www.delphion.com/details?pn=US04238491__
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Method for treating hypertension with nicotine Inventor(s): Emley; Grace S. (Augusta, MI), Hutchinson; Ronald R. (Augusta, MI) Assignee(s): Foundation for Behavioral Research (Augusta, MI) Patent Number: 4,748,181 Date filed: May 15, 1985 Abstract: Hypertension is treated by chronic administration of nicotine or pharmaceutically acceptable salt of nicotine. More specifically, essential hypertension is treated in primates using effective dosages of nicotine. Excerpt(s): This invention relates to a method of treating hypertension which comprises administering to a hypertensive subject requiring such treatment, nicotine or a pharmacologically acceptable acid addition salt of nicotine, for an extended period of time... Nicotine or nicotine related substances have previously been employed or proposed for employment as a treatment for colic (U.S. Pat. No. 101,145), tobacco substitute (U.S. Pat. Nos. 904,521 and 2,981,641), insecticide and parasiticide (U.S. Pat. No. 2,175,980), snake repellent (U.S. Pat. No. 3,069,314), antihistamine potentiator (U.S. Pat. No. 3,126,319), swine food additive (U.S. Pat. No. 3,252,802) and skin care agent (U.S. Pat. No. 2,437,561)... U.S. Pat. No. 3,870,794 discloses administering nicotine and related substances to ameliorate emotional disorders, such as anger, hostility, irritability and frustration. Web site: http://www.delphion.com/details?pn=US04748181__
Patents 293
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Method for treating ocular hypertension and glaucoma Inventor(s): Yokoyama; Tomihisa (Tokyo, JP), Yanagisawa; Hiroaki (Tokyo, JP), Hosokawa; Tsunemichi (Tokyo, JP) Assignee(s): Sankyo Company, Limited (Tokyo, JP) Patent Number: 5,925,664 Date filed: September 16, 1996 Abstract: A method of treating ocular hypertension and/or glaucoma in a mammal by locally administering to the eyes of a mammal a composition comprising an effective amount of a compound of the formula wherein R.sup.1 is lower alkyl, lower alkenyl, or R.sup.5 --A--B--, where R.sup.5 is hydrogen, lower alkyl, cycloalkyl or aliphatic acyl; A is oxygen or sulfur; and B is a single bond or a lower alkylene; R.sup.2 is lower alkyl, lower alkenyl, or --C(R.sup.6)(R.sup.7)(R.sup.8), wherein R.sup.6 is hydroxyl or lower alkoxy; and R.sup.7 and R.sup.8 each is hydrogen, lower alkyl, lower alkenyl, lower alkynyl, cycloalkyl, aryl or aralkyl; R.sup.3 is carboxyl or --CON(R.sup.9)(R.sup.10), wherein R.sup.9 and R.sup.10 each is hydrogen or lower alkyl; R.sup.4 is carboxyl, carboxycarbonyl or tetrazol-5-yl; or a pharmacologically acceptable salt or ester thereof. Excerpt(s): The present invention relates to an excellent ocular tension lowering agent and/or a glaucoma therapeutic agent for eye drops and/or relates to their uses as an ocular tension lowering agent and/or a glaucoma therapeutic agent for eye drops, and in addition relates to an excellent method of medical treatment administering the agent to mammals with ocular hypertension and/or with glaucoma diseases... Hitherto, the use of an angiotensin II inhibitor for the purpose of lowering ocular tension has been described in reports. However, there are a few cases where the effect has been certified in actual experiment, and only oral use of the inhibitor has been described... However, in order to use the inhibitor as eye drops, the effect of administering the inhibitor as eye drops in the invention disclosed in the aforesaid International Publication was not enough to use the inhibitor as a medicament. Web site: http://www.delphion.com/details?pn=US05925664__
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Method of alleviating hypertension Inventor(s): Wright; George C. (Norwich, NY), Butterfield; James L. (New Berlin, NY) Assignee(s): Morton-Norwich Products, Inc. (Norwich, NY) Patent Number: 4,071,632 Date filed: December 30, 1976 Abstract: 3-Amino-2-hydrazinopyridine hydrochloride is useful in the alleviation of hypertension. Excerpt(s): This invention is concerned with the treatment of hypertension. More particularly, it is concerned with a method of treating hypertension by the administration of 3-amino-2-hydrazinopyridine hydrochloride to a hypertensive host... The compound 3-amino-2-hydrazinopyridine hydrochloride has been described in U.S. Pat. No. 3,549,631... It has now been discovered that 3-amino-2-hydrazinopyridine hydrochloride when administered intraperitoneally, intravenously or orally to spontaneously hypertensive rats in a dose ranging from 0.1 to 100 mg/kg in a vehicle
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such as isotonic saline produced marked reduction in arterial blood pressure. The magnitude and duration of the antihypertensive effect elicited by this compound is dose dependent, lower dosages causing less and shorter time period reduction of blood pressure and larger dosages increasing the amount and time period of blood pressure lowering. Web site: http://www.delphion.com/details?pn=US04071632__ •
Method of controlling hypertension using monoclonal antibodies to angiotensin-II Inventor(s): Reilly; Thomas M. (Wilmington, DE) Assignee(s): E. I. Du Pont De Nemours and Company (Wilmington, DE) Patent Number: 4,911,909 Date filed: January 2, 1987 Abstract: Monoclonal antibodies to angiotensin II and the continuous hybrid monoclonal cell lines for their production are provided. These antibodies are useful in the diagnosis and treatment of angiotensin II-induced hypertension. Excerpt(s): This invention relates to hybrid cell lines (lymphocyte hybridomas) for the production of monoclonal antibodies to angiotensin II, to the homogenous monospecific antibodies, and their use in the diagnosis and treatment of angiotensin-induced hypertension... The renin-angiotensin system (RAS) is a major regulator of cardiovascular homeostasis. See, for example, Hypertension and the Angiotensin System-Therapeutic Approaches, A. E. Doyle and A. G. Bearn, ed., Raven Press, 1983, and references contained therein. In the RAS, angiotensin I (AI) is formed from angiotensinogen by the enzyme renin. AI, a decapeptide, is cleaved by converting enzyme to angiotensin II (AII), the effector molecule, which is an octapeptide. At least two compartments of AII, one localized in the plasma and the other localized in the vascular tissue, contribute towards the blood pressure elevation in various hypertensive states. An understanding of their relative contributions in these different states remains an important problem in the diagnosis and treatment of hypertension... Experimental and clinical studies of the RAS have been greatly aided by the development of pharmacologic inhibitors which interfere at various points in the system. For example, suppression of converting enzyme activity by inhibitors such as captopril and enalapril now represents an important approach to anti-hypertensive therapy. However this enzyme is capable of hydrolyzing many peptide substrates in addition to AII, including bradykinin, substance P, enkephalins and neurotensin; V. J. Dzau, J. Cardiovascular Pharmacol., 7, S53 (1985). Therefore inhibitors of the enzyme are unlikely to be physiologically specific with respect to the RAS. A lack of physiological specificity may also apply to inhibitors of the enzyme renin, a protease whose substrate specificity has recently been recognized to comprise more than just angiotensinogen; T. Inagami, K. Ohtuski, T. Inagami, J. Biol. Chem., 258, 7476 (1983). Since AII is the primary biologically active component of the RAS, an antagonist to this hormone should represent a physiologically specific inhibitor of the RAS. Current peptide antagonists of AII, such as saralasin ([Sar.sup.1, Ala.sup.8 ] AII) are limited in their use as RA inhibitors by their inherent partial agonist properties. Web site: http://www.delphion.com/details?pn=US04911909__
Patents 295
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Method of determining volume dependent hypertension via reduction in phosphorylation Inventor(s): Puschett; Jules B. (New Orleans, LA) Assignee(s): Tulane University Medical Center (New Orleans, LA) Patent Number: 6,251,611 Date filed: September 26, 1997 Abstract: A method of determining the presence of chronic volume dependent hypertension is provided wherein a determination is made as to whether there has been a substantial reduction in phosphorylation of the blood-derived protein or renal proximal brush border membrane protein and if such reduction exists concluding that chronic volume dependent hypertension exists in a patient. The method may advantageously be practiced by employing blood serum or blood plasma as the body specimen containing the protein in determining whether a patient has chronic volume dependent hypertension, a cellular component of the blood, such as a blood-derived protein coming from the plasma membrane of lymphocytes. The method may include subsequent therapeutic patient treatment. Related diagnostic apparatus is also provided. Excerpt(s): The present invention provides a means for determining whether a patient has volume dependent hypertension and, more specifically, it provides such a method based upon determining if a substantial reduction in phosphorylation of a specific protein exists. The invention also relates to a diagnostic apparatus employable in making such determination... Elevated blood pressure or hypertension has long been recognized as a health problem. It is a very common disease which can have widespread effects on a patient's body and frequently, unlike numerous other diseases, is asymptomatic... Despite known means of measuring blood pressure of a patient as by a sphygmomanometer, for example, there is lacking an accurate reliable means of detecting the presence of volume dependent hypertension involving higher arterial blood pressure by use of a body specimen, such as blood serum or blood plasma. Web site: http://www.delphion.com/details?pn=US06251611__
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Method of diagnosing and treating myocardial infarction and hypertension Inventor(s): Bagrov; Alexei Y. (St. Petersburg, RU) Assignee(s): Biomedical Sciences Research Laboratories, Inc. (Millersville, MD) Patent Number: 5,770,376 Date filed: March 2, 1995 Abstract: The present invention relates to methods for diagnosing acute myocardial infarction through the measurement of the level of marinobufagin-like immunoreactivity in the blood of patients suspected of this diagnosis; a method for treating patients with acute myocardial infarction with antibody to marinobufagin, a bufodienolide, to prevent the occurrence of cardiac arrhythmias; antibodies which specifically recognize marinobufagin or other bufodienolides; hybridomas producing these antibodies; a process for preparing such antibodies; and an immunoassay method for marinobufagin for research purposes using its specific antibody.The antibodies of the present invention make it possible to conveniently measure bufodienolides with specificity and high sensitivity. This is useful in determining the existence and degree of hypertension and myocardial infarction, and in treating myocardial infarction.
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Excerpt(s): Hypertension is the primary risk factor for coronary, cerebral and renal vascular diseases which cause over half of all deaths in the United States. It has been estimated that the number of hypertensive patients in the United States alone is substantially 57 million and on the rise. The widespread awareness of the danger of elevated blood pressure has become the most frequent reason for visits to physicians. No single or specific cause is known for the hypertension referred to as primary (essential) hypertension. Primary hypertension has been attributed to such causes as hemodynamic pattern, genetic predisposition, vascular hypertrophy, hyperinsulinemia, defects in cell transport or binding, defects in the reninangiotensin system (low-renin or high renin hypertension) and along with insulin, angiotensin and natriuretic hormone, catecholamines arising in response to stress are known to be pressor-growth promoters. Increased sympathetic nervous activity may raise the blood pressure in a number of ways, for example, either alone or in concert with stimulation of renin release by catecholamines, causing arteriolar and venous constriction, by increasing cardiac output, or by altering the normal renal pressure-volume relationship. Primary hypertension is also associated with, for example, obesity, sleep apnea, physical inactivity, alcohol intake, smoking, diabetes mellitus, polycythemia and gout. Secondary forms of hypertension may arise from oral contraceptive use and parenchymal renal disease: renovascular hypertension caused by, for example, atherosclerotic disease, tumors (renin-secretory tumors); Cushing's Syndrome; heart surgery; and pregnancy. Chronic hypertension and renal disease during pregnancy may progress into eclampsia, a primary cause of fetal death... It has been theorized that blood serum and various mammalian tissues contain a substance, biologically and immunoreactively, similar to digitalis glycosides and digoxin (ouabain)-like which have been labeled endogenous digoxin-like factors (EDLF). This theory has been supported in recent years by considerable evidence of a causal role for sodium in the genesis of hypertension. The evidence includes the finding of increased intracellular sodium in hypertensive mammals. Increases have also been noted in normotensive children of hypertensive parents. It has been discovered that an increased fluid volume stimulates the secretion of EDLF that inhibits the Na+,K+-ATPase pump. The inhibition is brought about by the reaction of the EDLF with the alpha-subunit of the ouabain-sensitive-magnesiumdependent, Na+,K+-ATPase in a manner similar to the digitalis glycosides. In the case of renovascular types of hypertension, inhibition of the sodium pump increases renal sodium excretion and restores vascular volume while at the same time leading to hypertension by increasing intracellular sodium content by potentiating preexisting vasoconstriction and finally initiating a new circle in the pathogenesis of hypertension. Increased plasma concentrations of EDLF have been discovered in hypertension caused by other physical and pathological conditions. Consequently, it was discovered that the administration of an antidigoxin antiserum to hypertensive animals causes a pronounced decrease in the blood pressure... The exact chemical nature, as well as the site of origin, of EDLF is not known. It has been proposed that endogenous digoxin is a peptide originating in the hypothalamus. It has also been reported that EDLF originates in the adrenals and the heart. It has been shown that the EDLF substance exists in several different molecular forms, at least one of the forms being steroidal in nature. Confirming this, it was discovered that several steroids with digitalis-like imnunoreactivity and ability to inhibit Na+,K+-ATPase were identified in various amphibian tissues. Web site: http://www.delphion.com/details?pn=US05770376__
Patents 297
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Method of reducing pulmonary hypertension and atrial fibrillation after surgery using cardiopulmonary bypass Inventor(s): Royston; David (Harefield, GB), Riedel; Bernhard (Harefield, GB), Marangos; Paul J. (La Costa, CA), Fox; Anthony W. (Rancho LaCosta, CA) Assignee(s): Cypros Pharmaceutical Corp. (Carlsbad, CA) Patent Number: 6,011,017 Date filed: April 15, 1998 Abstract: A method is disclosed for using fructose-1,6-diphosphate (FDP) to reduce and prevent two very serious problems caused by surgery that requires cardiopulmonary bypass. Before bypass begins, a liquid that contains FDP is intravenously injected into the patient, preferably over a period such as about 10 to 30 minutes, to allow the FDP to permeate in significant quantity into the heart and lungs while the heart is still beating. FDP can be added to the cardioplegia solution that is pumped through the heart to stop the heartbeat, and/or during bypass. This treatment was found to reduce two very important and serious problems that have unavoidably plagued CPB surgery in the past, which are: (1) elevated levels of pulmonary vascular resistance (PVR), which includes pulmonary hypertension; and (2) high occurrence rates for atrial fibrillation. Prior to this discovery, there has never been any satisfactory treatment which could reduce the severity and occurrence rates for these two major problems. FDP also can be co-administered in this manner, along with (1) a buffering or alkalizing agent that counteracts acidosis, such as sodium bicarbonate or THAM, and/or (2) a drug that reduces the formation of lactic acid, such as dichloroacetate. Excerpt(s): This invention relates to a method of using a drug to reduce and prevent two very serious problems that often arise as a result of surgery involving cardiopulmonary bypass... (7) surgery to correct a congenital heart disease, which is done most commonly in children. It should be noted that children who suffer from congenital heart disease that is sufficiently severe to require CPB surgery also tend to suffer from high rates of pulmonary hypertension... All of these types of surgery are described in various wellknown medical texts, such as Gibbon's Surgery of the Chest (Sabiston and Spencer, eds., Saunders Publ., Philadelphia, Pa.) and in various medical journals that are devoted to the subject of cardiac and/or thoracic surgery. Web site: http://www.delphion.com/details?pn=US06011017__
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Method of treating hypertension Inventor(s): Tokimitsu; Ichiro (Tochigi, JP), Suzuki; Atsushi (Tochigi, JP), Ochiai; Ryuji (Tochigi, JP) Assignee(s): KAO Corporation (Tokyo, JP) Patent Number: 6,310,100 Date filed: September 22, 2000 Abstract: A method for treating hypertension, a cardiac disease, or a cerebrovascular disease comprising administration of ferulic acid or a derivative thereof, to a subject in need of treatment. Therapeutic compositions comprising ferulic acid and its derivatives may comprise pharmaceutical products, nutritional supplements or products, and foods. Such compositions may further comprising diglycerides in combination with ferulic acid and its derivatives.
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Excerpt(s): The present invention is directed to methods of treating diseases such as hypertension using ferulic acid compounds. It also relates to compositions, such as fat compositions, comprising a ferulic acid compound and a diglyceride... Hypertension is correlated with cardiac diseases such as angina pectoris, myocardial infarction and heart failure. It also is associated with cerebrovascular diseases such as cerebral infarction, cerebral hemorrhage and subarachnoid hemorrhage. Cardiac diseases and cerebrovascular diseases are the second and third causes of death in Japan, respectively. Such diseases cause substantial mortality and morbidity in many other countries as well, particularly in the more developed parts of the world. In the year 1998, sixty four patients per thousand in Japan visited the hospital regularly for hypertension according to research by the Ministry of Health and Welfare and hypertension is a primary cause of death... As a countermeasure against the hypertension, a number of therapies have been developed, for instance development and use antihypertensive drugs such as diuretics, sympatholytic depressants, vasodilators and angiotensin converting enzyme inhibitors. These drugs are usually administered to patients diagnosed with a serious degree of hypertension. Web site: http://www.delphion.com/details?pn=US06310100__
Patent Applications on Hypertension As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to hypertension: •
Agent for preventing, improving or treating hypertension Inventor(s): Tokimitsu, Ichiro ; (Haga-gun, JP), Ochiai, Ryuji ; (Haga-gun, JP), Suzuki, Atsushi ; (Haga-gun, JP) Correspondence: OBLON SPIVAK MCCLELLAND MAIER & NEUSTADT PC; FOURTH FLOOR; 1755 JEFFERSON DAVIS HIGHWAY; ARLINGTON; VA; 22202; US Patent Application Number: 20020054923 Date filed: September 4, 2001 Abstract: The invention relates to an agent for preventing, improving or treating hypertension, which exhibits a hypotensive effect, inhibits the rise of blood pressure and improves hypertension, and food for preventing or improving hypertension, which does not become a burden in daily intake, has a higher antihypertensive effect and is useful as a diet during treatment for patients of hypertension. The agent for preventing, improving or treating hypertension contains the following components (A) and (B):(A) a compound selected from the group consisting of caffeic acid, chlorogenic acid and ferulic acid, and esters and pharmaceutically acceptable salts thereof; and(B) a component selected from the group consisting of central nervous system stimulating components, food fibers, extracts of perennial evergreen leaves of the genus Camellia, Theaceae, or Eucommia ulmoides Oliver, Eucommiae, organic acids having a molecular weight of 60 to 300 (excluding citric acid) and pharmaceutically acceptable salts thereof, and sugar alcohols.
10
This has been a common practice outside the United States prior to December 2000.
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Excerpt(s): The present invention relates to an agent for preventing, improving or treating hypertension, which permits inhibiting the rise of blood pressure and moreover improving hypertension and is useful as food and drink, and food such as food for specific health in addition to a drug for preventing, improving or treating hypertension... Cardiac diseases such as angina pectoris, myocardial infarction and heart failure, and cerebrovascular diseases such as cerebral infarction, cerebral hemorrhage and subarachnoid hemorrhage very closely relate to hypertension and stand second and third, respectively, in the Japanese causes of death. According to the basis research (the 1998 year) of the national life by the Ministry of Health and Welfare, the number of patients going to hospital regularly with hypertension is sixty-four per thousand in Japan and stands first in the cause of decease. As a countermeasure against the hypertension, may be mentioned the use of antihypertensive drugs such as diuretics, sympatholytic depressants, vasodilators and angiotensin converting enzyme inhibitors. These drugs are mainly applied to serious patients of hypertension. On the other hand, general treatments aiming at improving life custom, such as dietetic therapy, therapeutic exercise and restriction of smoking and drinking, are widely applied to slight and serious patients of hypertension. Therefore, the importance of general treatments is recognized. Among others, improvement in the custom of eating is said to be important, and there are many foods traditionally said to have a hypotensive effect. Antihypertensive materials derived from food have heretofore been extensively searched, and isolation and identification of active ingredients having a hypotensive effect have been made in large numbers. Juices of immature fruits of apple, sand pear, peach and the like, which belong to Rosaceae, contain fruit polyphenol having an inhibitory effect on an angiotensin I converting enzyme (ACE), and caffeic acid and chlorogenic acid have an ACE-inhibiting effect. It has been proposed to use such a fruit juice as an antihypertensive agent (Japanese Patent Application Laid-Open No. 259453/1996)... However, under the circumstances, many of drugs used for the purpose of treating hypertension are satisfactory in effectiveness, whereas patients are heavily burdened with their side effects, such as tachycardia and bradycardia, existing in no small numbers. With respect to foods said to have a hypotensive effect, or active ingredients thereof, the effectiveness is not always satisfactory. Further, many of them require a long time to develop a hypotensive effect. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Alkylaminoalkyl-sulfonyl-terminated Beta-alanineamide amino-diol compounds for treatment of hypertension Inventor(s): Hanson, Gunnar J. ; (Skokie, IL), Chen, Barbara B. ; (Glenview, IL), Baran, John S. ; (Winnetka, IL) Correspondence: Pharmacia Corporation; Corporate Patent Department; P. O. Box 5110; Chicago; IL; 60680; US Patent Application Number: 20010011101 Date filed: January 17, 2001 Abstract: Compounds characterized generally as alkylaminoalkyl-terminated .beta.alanineamide amino diol derivatives are useful as renin inhibitors for the treatment of hypertension. Compounds of particular interest are those of the formula 1wherein n is two or three; wherein x is a number selected from zero, one and two; wherein R.sup.2 is selected from hydrido, methyl, ethyl and phenyl; wherein R.sup.3 is selected from hydrido, cyclohexylmethyl, benzyl, fluorobenzyl, chlorobenzyl, napthylmethyl,
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fluoronaphthylmethyl and chloronaphthylmethyl; wherein R.sup.5 is methyl; wherein R.sup.7 is cyclohexylmethyl; wherein R.sup.8 is selected from n-propyl, isobutyl, cyclopropyl, cyclopropylmethyl, allyl and vinyl; and wherein each of R.sup.9 and R.sup.10 is a group independently selected from methyl, ethyl and isopropyl; or a pharmaceutically-acceptable salt thereof. Excerpt(s): Renin-inhibiting compounds are known for control of hypertension. Of particular interest herein are compounds useful as renin inhibiting agents... Renin is a proteolytic enzyme produced and secreted into the bloodstream by the juxtaglomerular cells of the kidney. In the bloodstream, renin cleaves a peptide bond in the serum protein angiotensinogen to produce a decapeptide known as angiotensin I. A second enzyme known as angiotensin converting enzyme, cleaves angiotensin I to produce the octapeptide known as angiotensin II. Angiotensin II is a potent pressor agent responsible for vasoconstriction and elevation of cardiovascular pressure. Attempts have been made to control hypertension by blocking the action of renin or by blocking the formation of angiotensin II in the body with inhibitors of angiotensin I converting enzyme... Classes of compounds published as inhibitors of the action of renin on angiotensinogen include renin antibodies, pepstatin and its analogs, phospholipids, angiotensinogen analogs, pro-renin related analogs and peptide aldehydes. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Anti-hypertensive composition and methods of treatment Inventor(s): Bergeron, Raymond J. JR. ; (Gainesville, FL) Correspondence: Miles & Stockbridge; Suite 500; 1751 Pinnacle Drive; McLean; VA; 22102-3833; US Patent Application Number: 20020132815 Date filed: March 7, 2002 Abstract: Pharmaceutical compositions for the treatment of hypertension comprising an effective anti-hypertensive amount of at least one compound in association with a pharmaceutically acceptable, substantially non-toxic carrier or excipient, the compound having one of the formulae (I), (II), (III) or (IV), and methods for the treatment of hypertension or effecting anti-hypertensive action which comprises administering to a patient requiring anti-hypertensive therapy or effect at least one of the above-described compounds. Excerpt(s): This application contains subject matter related to that contained in the following patent applications, the entire contents and disclosures of all of which are incorporated herein by reference: Ser. Nos. 06/746,672 filed Jun. 20, 1985 (abandoned); 07/313,734 filed Feb. 22, 1989 (U.S. Pat. No. 5,128,353); 07/645,644 filed Jan. 25, 1991 (U.S. Pat. No. 5,173,505); 07/993,620 filed Dec. 21, 1992 (U.S. Pat. No. ______); 06/936,835 filed Dec. 2, 1986 (abandoned); 06/066,227 filed Jun. 25, 1987 (abandoned); 07/210,520 filed Jun. 23, 1988 (U.S. Pat. No. 5,091,576); 07/834,345 filed Feb. 12, 1992 (U.S. Pat. No. ______); 07/870,441 filed Oct. 9, 1992; 07/986,576 filed Dec. 7, 1992; 08/061,707 filed May 17, 1993; 08/124,557 filed Sep. 22, 1993; and 08/162,776 filed Dec. 8, 1993... The present invention relates to novel anti-hypertensive compositions and methods of treating hypertension wherein the active anti-hypertensive agent is one of several classes of polyamines and certain derivatives thereof... (IV) a salt of (I), (II) or (III) with a pharmaceutically acceptable acid. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Combination therapy for hypertension Inventor(s): Sartani, Abraham ; (Arese, IT), Leonardi, Amedeo ; (Milan, IT), Sironi, Giorgio ; (Pieve Emanuele, IT) Correspondence: DARBY & DARBY P.C.; Post Office Box 5257; New York; NY; 101505257; US Patent Application Number: 20030180355 Date filed: October 16, 2002 Abstract: Disclosed are compositions and methods for treating hypertension comprising enalapril and lercanidipine in amounts effective in combination to reduce blood pressure to a patent in need of treatment. Excerpt(s): The present application claims priority under 35 U.S.C. 119 (e) of U.S. provisional application 60/344,601, filed Oct. 23, 2001 and priority under 35 U.S.C. 119 (a)-(d) of Italian patent applications MI 2001A 012136 filed Oct. 16, 2001. Each of the aforementioned applications is hereby incorporated herein by reference in its entirety... The present invention contemplates a method for treating hypertension with a combination of enalapril and lercanidipine... Hypertension is one of the most common cardiovascular disease states. In the United States, over 50 million people have been diagnosed with hypertension (which is defined as a blood pressure greater than or equal to 140/90 mm Hg). Elevated arterial pressure can cause pathological changes in the vasculature and hypertrophy of the left ventricle. Due to the damage that can be produced by hypertension, it is proposed to be the principal cause of stroke, myocardial infarction, and sudden cardiac death. Additionally, it is believed to be a major contributor to cardiac failure, renal insufficiency, and dissecting aneurysm of the aorta. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Compositions and methods for alleviating hypertension or preventing a rise in blood pressure Inventor(s): Suzuki, Atsushi ; (Chuo-ku, JP), Tokimitsu, Ichiro ; (Chuo-ku, JP), Ochiai, Ryuji ; (Chuo-ku, JP) Correspondence: OBLON SPIVAK MCCLELLAND MAIER & NEUSTADT PC; FOURTH FLOOR; 1755 JEFFERSON DAVIS HIGHWAY; ARLINGTON; VA; 22202; US Patent Application Number: 20020051810 Date filed: August 7, 2001 Abstract: Products and compositions for preventing or reducing the severity of hypertension. These products contain (a) ferulic acid or a ferulate ester, and (b) caffeic acid and/or a chlorogenic acid. The preventive or remedy can suppress a rise in blood pressure and alleviate hypertension, and is usable as a food. Excerpt(s): The present invention relates to products and compositions that prevent, remedy or reduce the severity of hypertension and that are capable of suppressing a rise in blood pressure... Hypertension in Japan ranks first among reasons why patients attend hospitals. According to the National Life Fundamental Survey of Ministry of Health and Welfare (fiscal 1998), in Japan, 64 patients per 1000 were admitted to hospitals for hypertension... Heart diseases such as angina pectoris, myocardial
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infarction and heart failure and cerebrovascular diseases such as cerebral infarction, cerebral hemorrhage and subarachnoid hemorrhage are closely related to hypertension and rank second and third, respectively, among the causes of death of the Japanese. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Compositions and methods for the treatment of glaucoma or ocular hypertension Inventor(s): Plourde, Robert JR. ; (Chapel Hill, NC), Yerxa, Benjamin R. ; (Raleigh, NC), Brown, Edward G. ; (Apex, NC), Boyer, Jose L. ; (Chapel Hill, NC) Correspondence: HOWREY SIMON ARNOLD & WHITE, LLP; BOX 34; 301 RAVENSWOOD AVE.; MENLO PARK; CA; 94025; US Patent Application Number: 20020128224 Date filed: February 27, 2002 Abstract: The present invention is directed to a method of reducing intraocular pressure. The method comprises administering to a subject a pharmaceutical composition comprising an effective amount of a nucleoside 5'-pyrophosphate pyranoside or analogue, which is defined by general Formula I. The method of the present invention is useful in the treatment or prevention of ocular hypertension, such as found in glaucoma, including primary and secondary glaucoma. The method can be used alone to reduce intraocular pressure. The method can also be used in conjunction with another therapeutic agent or adjunctive therapy commonly used to treat glaucoma to enhance the therapeutic effect of reducing the intraocular pressure. The present invention also provides a novel composition comprising a nucleoside 5'-pyrophosphate pyranoside or analogues. Excerpt(s): This application is a continuation-in-part of U.S. application Ser. No. 09/934,970, filed Aug. 21, 2001; which is a continuation-in-part of U.S. application Ser. No. 09/643,138, filed Aug. 21, 2000... This invention relates to a method of lowering intraocular pressure and thereby treating ocular hypertension and/or glaucoma... Glaucoma is a slowly progressive blinding disease usually associated with chronic elevation of intraocular pressure (IOP). Sufficiently high and persistent intraocular pressure is believed to result in damage to the optic disc at the juncture of the optic nerve and retina, resulting in degeneration of retinal ganglion cells and blindness characteristic of glaucoma. However, the mechanism whereby IOP elevation (also known as ocular hypertension) leads to glaucoma is not well understood. Additionally, a fraction of patients with typical visual field loss associated with glaucoma do not show abnormal elevated IOP levels (known as low-tension or normal-tension glaucoma). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Compositions methods and kits relating to treating and diagnosing hypertension Inventor(s): Lifton, Richard P. ; (Guilford, CT), Choate, Keith ; (New Haven, CT), Wilson, Frederick H. ; (New Haven, CT), Nelson-Williams, Carol ; (Hamden, CT), Ishikawa, Kazuhiko ; (Toyonaka City, JP) Correspondence: MORGAN, LEWIS & BOCKIUS LLP; 1701 MARKET STREET; PHILADELPHIA; PA; 19103-2921; US Patent Application Number: 20030082720 Date filed: July 17, 2002 Abstract: The present invention relates to novel nucleic acids encoding a mammalian WNK, and proteins encoded thereby, preferably, human WNK1 and human WNK4. These novel nucleic acids, and mutant forms thereof, are associated with, inter alia, renal electrolyte handling, hypertension, and pseudohypoaldosterism type II (PHA II). That is, the present invention relates to novel mutations (e.g., deletions and missense mutations in an exon, intron, or both, of a nucleic acid encoding a WNK) that mediate and/or are associated with altered expression, among other things. These mutations are, in turn, associated with and/or mediate disease (e.g., hypertension, PHA II, and the like). Thus, these nucleic acids provide a novel target for treatment, diagnosis, and development of therapeutics to treat these diseases. Excerpt(s): This application is entitled to priority pursuant to 35 U.S.C.sctn.119(e) to U.S. Provisional Patent Application No. 60/306,084, which was filed on Jul. 17, 2001... Hypertension, or high blood pressure, is often referred to as the silent killer in that a hypertensive patient often exhibits no specific symptoms, yet hypertension is a prominent risk factor for many disabling and often fatal diseases, including stroke, myocardial infarction, arrhythmia, congestive heart failure, renal failure and retinopathy. It is estimated that 50 million Americans have high blood pressure... Hypertension is classified as either essential hypertension or secondary hypertension. The former is the most common, with hypertension as the only symptom and no known underlying cause. Secondary hypertension is classified as hypertension with a known underlying medical condition responsible for the hypertensive state. The predisposing conditions may include renal disease, endocrine system abnormalities, adrenal or pituitary tumors, blood vessel irregularities, medications, and as recently discovered, genetic factors. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Detection of hypertension using immunoreactive metabolic products Inventor(s): Kim, Hyesook ; (Bloomfield Hills, MI), Capdevila, Jorge H. ; (Nashville, TN), Novak, Raymond R. ; (West Bloomfield, MI), Kroetz, Deanna ; (San Francisco, CA) Correspondence: KOHN & ASSOCIATES; 30500 Northwestern Highway, Suite 410; Farmington Hills; MI; 48334; US Patent Application Number: 20020025544 Date filed: September 4, 2001 Abstract: A method to assess hypertension by measuring the amount of free and conjugated hydroxyeicosatrienoic acids (DHETs) and metabolites of DHETs, which are metabolites of arachidonic acid (AA) epoxygenases and epoxide hydrolases, in a biological sample which contains the DHETs (using any methods including GC/MS or
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ELISA) is disclosed. The method further included determining the amount of molecules containing a DHET-specific epitope immunoreactive with antibodies produced against DHETs present in the sample. This amount is compared with a control sample(s). Hypertension is determined through the comparison wherein the amount of increase of free and conjugated DHETs and metabolites of DHETs in the sample isolated from an organism. The present invention also provides a method to assess catalytic activity of AA epoxygenases using immunoassays by subtracting the amounts of NADPHindependent epoxyeicosatriencic acids (EETs) from total (NADPHdependent+independent) EETs. The present invention also provides a method to decrease hepatic M epoxygenase expression including 2C23 by treatment of rats with a glucocorticoid including dexamethasone. Excerpt(s): This application is a conversion of U. S. Provisional Patent Application Ser. No. 60/136,475, filed May 28, 1999, claiming benefit under 35 U.S.C.sctn.119 (e), and which is incorporated herein by reference... This invention relates to a method to analyze arachidonic acid (AA)-derived products which are immunoreactive with antibodies produced against hydroxyeicosatrienoic acids (DHETs). More specifically, the present invention relates to a method which can be used to facilitate investigations of the physiological and pathophysiological roles of the metabolic products of arachidonic acid epoxygenases and epoxide hydrolases. The present invention also relates to a method to assess catalytic activity of AA epoxygenases using immunoassays and a method to decrease hepatic AA epoxygenase expression by treatment with glucocorticoids... AA is a component of cellular membranes and plays a critical role as a mediator of cell and organ function through its metabolic cascade. The AA cascade includes prostaglandin-synthases, lipoxygenases, and cytochromes P450 (CYPs). The CYP pathway is composed of lipoxygenases-like (allylic oxidation), .omega./.omega.-1 oxygenases and epoxygenases (olefin epoxidation), which metabolize AA to produce 5-, 8-, 9-, 11-, 12-, and 15-hydroxyeicosatetraenoic acids (HETEs), 16- to 20hydroxyeicosatetraenoic acids (OH--AAs), and 5,6-, 8,9-, 11,12- and 14,15epoxyeicosatrienoic acids (EETs), respectively (1). Epoxide hydrolases hydrolyze biologically active EETs to their corresponding dihydroxyeicosatrienoic acids (DHETs). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Genes and proteins predictive and therapeutic for stroke, hypertension, diabetes and obesity Inventor(s): Shimkets, Richard A. ; (West Haven, CT) Correspondence: MINTZ, LEVIN, COHN, FERRIS,; GLOVSKY AND POPEO, P.C.; One Financial Center; Boston; MA; 02111; US Patent Application Number: 20030055019 Date filed: July 15, 2002 Abstract: Common human diseases like diabetes and hypertension have been demonstrated to possess an associated genetic component composed of numerous underlying genetic defects. Traditional positional cloning of genes which possess the mutations responsible for complex disease has been hindered by both the low statistical power each locus may afford, and by the technically-laborious nature of the positional cloning methodologies. Disclosed herein is a methodology for the rapid identification of the genes responsible for quantitative trait loci (QTL) comprised of comprehensive gene expression analysis in organs relevant to disease in combination with the positional mapping of known QTL, so as to quantitatively identify candidate genes. This
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aforementioned methodology was applied to a total of five tissues/organs derived from the spontaneously hypertensive rat (SHR), the stroke-prone variant of the SHR (SHR-SP) and control Wistar Kyoto rats (WKY). Collectively these animals vary genetically in their predisposition to stroke, insulin sensitivity, blood pressure and body weight. These traits segregate into more than a dozen identified. The present invention discloses the differential-expression of sixty genes by GeneCalling.RTM. within five different tissues/organs among these animals. Additionally, five of the sixty genes were demonstrated to be localized within chromosomal regions linked to these traits of interest and possess amino acid substitutions which may contribute to the phenotype. Excerpt(s): The present invention discloses a set of genes which have been demonstrated to be anomalously regulated (i.e., dysregulated) in a model of combining a pathophysiological predisposition towards stroke, hypertension, diabetes and obesity. The present invention also relates to methods of treating and/or preventing stroke, hypertension, diabetes or obesity by the administration of the nucleic acids or protein products (and derivative and analogs thereof) of the GENE SET which are defective and/or are of low abundance in humans. The present invention further relates to methodologies of diagnosis, prognosis and screening for alleles of the GENE SET which may cause or predispose to the aforementioned diseases... Prevalent human diseases such as hypertension, non-insulin dependent diabetes (NIDDM), stroke, and obesity (dyslipidemia) have been shown to possess a significant genetic component composed of multiple, perhaps numerous, underlying genetic defects. Human Metabolic Syndrome X, a relatively common but poorly understood disorder, has been shown to possess a significant genetic component which is comprise of an association of the pathophysiologies of hypertension, insulin resistance, dyslipidemia and abdominal obesity. See e.g., Ferrannini, et al., 1987. New Engi. J Med. 317:350-357; Kaplan, 1989. Arteriosclerosis 9:335-344. Given the prevalence of this combination of diseases, many research groups have focussed their efforts upon determining the etiology (i.e., the primary causative genetic defects) of Metabolic Syndrome X in humans and closelyassociated animal models... The most successfully studied of these aforementioned diseases to date is hypertension, with strong evidence nucleotide sequence variants, with their associated amino acid residue substitutions, within a total of 11 human genes affect blood pressure. See e.g., Shimkets, et al., 1994. Cell 79(3):407-414; Simon, et al., 1997. Nat. Genet. 17(2):171-178; Geller, et al, 1998. Nat. Genet. 19(3):279-281. While in all probability these variants, in toto, account for only a fraction of the variation in blood pressure within the general population, they, nonetheless, serve to illustrate the potential that the etiology of many such diseases may involve the interaction of a large number of genetic components. As the majority of the genetic components of complex diseases such as human Metabolic Syndrome X have yet to be elucidated, a comprehensive analysis for the genetic defects responsible for the phenotype was undertaken in the present invention within a closely-associated animal model of this syndrome. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Hypertension-treatment composition containing panax notoginseng and salvia miltiorhiza and method of preparing same Inventor(s): Hong, Eun Kyung ; (Seoul, KR), Chung, Young Shin ; (Seoul, KR) Correspondence: LOWE HAUPTMAN GOPSTEIN; GILMAN & BERNER, LLP; SUITE 310; 1700 DIAGONAL ROAD; ALEXANDRIA; VA; 22314; US Patent Application Number: 20030003165 Date filed: June 14, 2001 Abstract: A composition for treating hypertension and lowering cholesterol is provided which contains the mixed extract of Panax notoginseng and Salvia miltiorrhiza as an active ingredient thus lowering and maintaining blood pressure substantially constant. Also provided is a method for preparing composition containing the mixed extract of Panax notoginseng and Salvia miltiorrhiza as an active ingredient. Excerpt(s): The present invention relates to a composition for treating hypertension and lowering cholesterol and a method for preparing same. More specifically, the present invention relates to a composition for treating hypertension and lowering cholesterol which contains the mixed extract of Pana notoginseng and Salvia miltiorrhiza as an active ingredient, and a method for preparing same... Cardiac and vascular diseases are one of the main causes of human death, and are represented by cerebral hemorrhage, cerebral thrombosis, heart failure, cardiac infarction, etc. However, etiology of such diseases is very diverse and complex. The target for treatment of hypertension is to prevent the occurrence of complications in brain, heart, kidney, liver, etc., thereby allowing the human to manage a normal life by the average life span. The development of drugs for treatment of hypertension is still urgently required... Blood pressure and hypertension will be more specifically explained hereinbelow. The term, blood pressure, denotes a pressure of blood stream flowing through blood vessels, i.e., arterial pressure. In this context, the term, hypertension, means that a certain cause induces an increase of resistance on the internal wall of blood vessel thus resulting in the maximum blood pressure (systolic blood pressure or highest blood pressure) of 150-160 mmHg and the minimum blood pressure (diastolic blood pressure or lowest blood pressure) of 90 mmHg or more. The former is called a systolic hypertension and the latter is called a diastolic hypertension. Although both may separately arise, it is general that they are simultaneously present. Moreover, hypertension may occur in the thirties, but it mainly occurs during the pre- and post-climacteric period in men rather than women. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Inhibitors of epoxide hydrolases for the treatment of hypertension Inventor(s): Morisseau, Christophe ; (West Sacramento, CA), Hammock, Bruce D. ; (Davis, CA), Zeldin, Darryl C. ; (Chapel Hill, NC), Kroetz, Deanna L. ; (San Francisco, CA) Correspondence: TOWNSEND AND TOWNSEND AND CREW, LLP; TWO EMBARCADERO CENTER; EIGHTH FLOOR; SAN FRANCISCO; CA; 94111-3834; US Patent Application Number: 20030119900 Date filed: December 23, 2002 Abstract: The invention provides compounds that inhibit epoxide hydrolase in therapeutic applications for treating hypertension. A preferred class of compounds for
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practicing the invention have the structure shown by Formula 1 1wherein Z is oxygen or sulfur, W is carbon phosphorous or sulfur, X and Y is each independently nitrogen, oxygen, or sulfur, and X can further be carbon, at least one of R.sub.1-R.sub.4 is hydrogen, R.sub.2 is hydrogen when X is nitrogen but is not present when X is sulfur or oxygen, R.sub.4 is hydrogen when Y is nitrogen but is not present when Y is sulfur or oxygen, R.sub.1 and R.sub.3 is each independently C.sub.1-C.sub.20 substituted or unsubstituted alkyl, cycloalkyl, aryl, acyl, or heterocyclic. Excerpt(s): This application is a continuation in part of U.S. Ser. No. 09/252,148, filed Feb. 18, 1999, the entire disclosure of which is incorporated herein by reference... The present invention generally relates to methods of treating hypertension using inhibitors of epoxide hydrolases. Preferred inhibitors include compounds, such as ureas, amides, and carbamates that can interact with the enzyme catalytic site and mimic transient intermediates. Other useful inhibitors include glycodiols and chalcone oxides which can interact with the enzyme as irreversible inhibitors... A combination of genetic and environmental factors contribute to the development of hypertension and its successful treatment is limited by a relatively small number of therapeutic targets for blood pressure regulation. Renal cytochrome P450 (CYP) eicosanoids have potent effects on vascular tone and tubular ion and water transport and have been implicated in the control of blood pressure (Makita et al. FASEB J 10: 1456-146, (1996)). The major products of CYP-catalyzed arachidonic acid metabolism are regio- and stereoisomeric epoxyeicosatrienoic acids (EETs) and 20-hydroxyeicosatetraenoic acid (20-HETE). 20HETE produces potent vasoconstriction by inhibition of the opening of a largeconductance, calcium-activated potassium channel leading to arteriole vascular smooth muscle depolarization (Zou et al. Am J. Physiol. 270:R228-237 (1996)). In contrast, the EETs have vasodilatory properties associated with an increased open-state probability of a calcium-activated potassium channel and hyperpolarization of the vascular smooth muscle and are recognized as putative endothelial derived hyperpolarizing factors (Campbell et al. Cir. Res. 78:415-423 (1996)). Hydrolysis of the EETs to the corresponding dihydroxyeicosatrienoic acids (DHETs) is catalyzed largely by soluble epoxide hydrolase (sEH) (Zeldin et al. J. Biol. Chem. 268:6402-64-07 (1993)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Internal 1, 15-lactones of fluprostenol and related prostaglandin F2a analogs and their use in the treatment of glaucoma and intraocular hypertension Inventor(s): Maxey, Kirk M. ; (Fort Collins, CO), Stanton, Michelle L. ; (Ann Arbor, MI) Correspondence: Benita J. Rohm; Rohm & Monsanto, P.L.C.; 660 Woodward Ave, Suite 1525; Detroit; MI; 48226; US Patent Application Number: 20010046982 Date filed: February 1, 2001 Abstract: Novel derivatives of prostaglandin compounds of the F-series (PGF), specifically macrocyclic internal 1,15-lactones of fluprostenol and related PGF analogs, such as cloprostenol or latanoprost. The novel analogs can be formulated into ophthalmic solutions and topically applied for the treatment of the increased intraocular pressure caused by glaucoma and the reduction of ocular hypertension. Excerpt(s): The present invention relates to novel derivatives of prostaglandin compounds of the F-series (PGF), and more particularly to internal 1,15-lactones of fluprostenol and related PGF analogs, and the use of such analogs for the treatment of
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increased intraocular pressure, such as that caused by glaucoma and the reduction of ocular hypertension... The prostaglandins are a family of 20 carbon atom fatty acids, being structural derivatives of prostanoic acid, which exhibit useful activity in a wide variety of biological systems. Accordingly, prostaglandins represent useful pharmacological agents in the treatment and prevention of a wide variety of disease conditions. For a fuller discussion of prostaglandins and their uses, see Oates, et al., New England J. Med., Vol. 319, No. 11, pp. 689-698 and Vol. 319, No. 12, pp. 761-768 (1988) and the references cited therein... Prostaglandin F.sub.2.alpha. (PGF.sub.2.alpha.) is a naturally-occurring prostaglandin which is widely manufactured and sold under a variety of trade names as an abortifacient, among other uses. See monograph 8065, page 1354 of The Merck Index, 12.sup.th edition (1996). It is also well known in the art that naturally-occurring prostaglandins can be topically applied to lower intraocular pressure. However, naturally-occurring prostaglandins generally cause inflammation and surface irritation of the eye. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Materials and methods for the treatment of hypertension and angina Inventor(s): Druzgala, Pascal ; (Santa Rosa, CA), Pfister, Jurg ; (Los Altos, CA), Zhang, Xiaoming ; (Campbell, CA), Milner, Peter G. ; (Los Altos Hills, CA) Correspondence: SALIWANCHIK LLOYD & SALIWANCHIK; A PROFESSIONAL ASSOCIATION; 2421 N.W. 41ST STREET; SUITE A-1; GAINESVILLE; FL; 326066669 Patent Application Number: 20030130330 Date filed: October 10, 2002 Abstract: The subject invention provides useful and novel calcium channel blockers based upon mibefradil. The subject invention also provides methods for synthesizing the compounds of the invention. The invention also provides methods for the control or prevention of hypertension, angina pectoris, ischemia, arrhythmias, and cardiac insufficiency in a patient by administering a compound, or composition, of the invention to an individual in need of such treatment. Excerpt(s): This application claims the benefit of U.S. Provisional Application Serial No. 60/328,588, filed Oct. 10, 2001... Adverse drug-drug interactions (DDI), elevation of liver function test (LFT) values, and QT prolongation leading to torsades de pointes (TDP) are three major reasons why drug candidates fail to obtain FDA approval. All these causes are, to some extent metabolism-based... Oxidative metabolism is the primary metabolic pathway by which most drugs (xenobiotics) are eliminated. It is also the major source of drug toxicity, either intrinsic toxicity or toxicity due to drug-drug interactions (DDI). Adverse DDI as well as intrinsic toxicity due to metabolites are a major reason for the failure of drug candidates in late-stage clinical trials. Many DDI are metabolism based, i.e., two or more drugs compete for the same metabolizing enzyme in the cytochrome P450 system (CYP450) [Guengerich, F. P. (1997) Role of cytochrome P450 enzymes in drug-drug interactions. In: Drug-drug interactions: scientific and regulatory perspectives. Li, A P (ed.)Academic Press, San Diego pp7-35 and Shen, W. W. (1995) Int. J. Psychiatry Med. 25:277-290]. Non-oxidative metabolic systems, such as hydrolytic enzymes, on the other hand, do not depend on co-factors; are not inducible; have a high substrate capacity; do not have a high degree of inter-individual variations in man; and are present in most tissues and organs. Non-oxidative metabolic systems are, therefore, much more reliable.
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Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Medicament for treatment of non-insulin dependent diabetes mellitus, hypertension and/or the metabolic syndrome Inventor(s): Jeppesen, Per ; (Ega, DK), Hermansen, Kjeld ; (Ega, DK), Gregersen, Soren ; (Ega, DK) Correspondence: WINSTON & STRAWN; PATENT DEPARTMENT; 1400 L STREET, N.W.; WASHINGTON; DC; 20005-3502; US Patent Application Number: 20030060428 Date filed: July 31, 2002 Abstract: A substance including the chemical structures of bicyclo [3.2.1]octan or the chemical structures of kaurene for the use in a dietary supplementation or as a constituent in a medicament for the treatment of non-insulin dependent diabetes mellitus, hypertension and/or the metabolic syndrome. The unique chemical structures of bicyclo [3.2.1]octan alone or in a kaurene structure provides the substances, such as e.g. steviol, isosteviol and stevioside with the capability of enhancing or potentiating the secretion of insulin in a plasma glucose dependent manner. The substances including these unique chemical structures also have the capability of reducing the glucagon concentration in the blood and/or lowering the blood pressure thereby providing a selfregulatory treatment system for non-insulin dependent diabetes mellitus and/or hypertension. In a combination drug which also comprise a soy protein, and/or soy fiber and/or at least one isoflavone these substances act synergistically and such combination drugs are highly useful both prophylacticly or directly in the treatment of e.g. the metabolic syndrome and obesity and has due to the self-regulatory effect a widespread applicability as a dietary supplementation. Excerpt(s): This application is a continuation of the U.S. national stage designation of International application PCT/DK01/00075 filed Feb. 1, 2001, the entire content of which is expressly incorporated herein by reference thereto... The present invention relates to a new medicament for the treatment of non-insulin dependent diabetes mellitus, hypertension, metabolic syndromes and other conditions in mammals... Diabetes is a common disease that has a prevalence of 2-4% in the population. Noninsulin dependent diabetes mellitus comprises about 85% of diabetes most commonly occurring at the age above 40 years. The incidence of non-insulin dependent diabetes mellitus is increasing and is at a global level expected to surpass 200 million subjects at year 2010. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method and compositions for treating persistent pulmonary hypertension using aralkyl ester soft drugs Inventor(s): Erhardt, Paul W. ; (Sylvania, OH), Aouthmany, Moustafa M. ; (Sylvania, OH) Correspondence: EMCH, SCHAFFER, SCHAUB & PORCELLO CO; P O BOX 916; ONE SEAGATE SUITE 1980; TOLEDO; OH; 43697 Patent Application Number: 20030130236 Date filed: November 18, 2002
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Abstract: A method and compositions for treating persistent pulmonary hypertension in human newborns that deploys an intravenous infusion of a modified drug formed by adding one or more of a predetermined chemical arrangement to an efficacious parent drug compound so as to retain efficacy while re-directing a preferred route and rate of the parent drug compound's metabolism to an inactive or very weakly active and nontoxic metabolite are disclosed. The chemical arrangement is 1wherein .phi. is a phenyl, substituted aryl or heteroaryl system that is already present in the parent drug compound or is specifically added to the parent drug compound via a metabolically stable connection;R is an alkyl or alkene containing chain either branched or unbranched from 0 to 10 carbons that is already present in the parent drug compound or is added to the parent drug compound via a metabolically stable connection to .phi.;X is a carboxyl, sulfoxyl or phosphatyl function that is specifically added to the parent drug compound via a metabolically stable connection to R; and,R' is an added alkyl, alkenyl or aralkyl group either branched or unbranched containing from 1 to 10 carbons, or is a structural element already present as an inherent portion of the parent drug compound. Excerpt(s): The present invention is a continuation-in part of U.S. Ser. No. 09/570,485 filed May 12, 2000, still pending, which is expressly incorporated herein by reference... Pharmaceutical agents or drugs exhibit desirable therapeutic properties because they contain distinct molecular arrangements called pharmacophores. Oftentimes, however, the pharmacophores or the presence of other chemical components within such compounds, provide a less than ideal overall profile relative to the final deployment of a given drug for a particular clinical indication. In some cases this situation can be improved by altering chemical features associated with a drug's distribution, metabolism or elimination (DME). This process, when successful, results in what is now referred to in the pharmaceutical community as a "soft drug" version of the original or parent drug compound: Soft Drugs. XX. Design, Synthesis and Evaluation of Ultra-Short Acting beta-Blockers, H.-S. Yang, W.-M, Wu and N. Bodor, Pharm. Res., 12, 329 (1995); and Synthesis and Enzymatic Hydrolysis of Esters, Constituting Simple Models of Soft Drugs, M. Graffner-Nordberg, K. Sjodin, A. Tunek and A. Hallberg, Chem. Pharm. Bull., 46, 591 (1998)... However, unless there is compelling preclinical data which suggests that the clinical application of a lead compound is going to become problematic, DMErelated features are typically not rigorously evaluated in a chemical manner during the early process of new drug discovery and development. This situation has arisen, in part, because substantial clinical experience is often required to accurately define the sometimes subtle parameters of an undesirable DME feature relative to the beneficial aspects of a new drug while the latter is within the close purview of its actual clinical use in a specific pathophysiological setting. The problem of not knowing exactly what DME and toxicity-related properties may need to be addressed is additionally confounded by not having ready chemical blueprints for how to generally proceed even when a particular DME or toxicity issue becomes suspected. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method for detecting a risk of hypertension and uses thereof Inventor(s): Salonen, Jukka T. ; (Jannevirta, FI) Correspondence: BIRCH STEWART KOLASCH & BIRCH; PO BOX 747; FALLS CHURCH; VA; 22040-0747; US Patent Application Number: 20030003470 Date filed: February 20, 2002
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Abstract: This invention relates to a method for detecting a risk of hypertension and for targeting antihypertensive treatment in a subject, the method comprising isolating genomic DNA from said subject, determining the DNA sequence comprising a nucleotide sequence encoding a variant .alpha..sub.2B-adrenoceptor protein. Excerpt(s): This invention relates to a method for detecting or diagnosing a risk of, or predisposition to, hypertension in a subject, for targeting antihypertensive treatment in a subject and for selecting subjects for studies testing antihypertensive agents... The publications and other materials used herein to illuminate the background of the invention, and in particular, to provide additional details with respect to the practice, are incorporated by reference... The .alpha..sub.2-adrenoceptors (.alpha..sub.2-ARs) mediate many of the physiological effects of the catecholamines norepinephrine and epinephrine. Three genetic subtypes of .alpha..sub.2-adrenoceptors are known in humans and other mammals, denoted as .alpha..sub.2A-, .alpha..sub.2B- and .alpha..sub.2C-adrenoceptors. The human genes encoding the receptors are located on chromosomes 10, 2 and 4, respectively. No splice variants are known to exist of these receptors, as the genes are intronless. The tissue distributions and physiological and pharmacological functions of the receptor subtypes have been reviewed e.g. by MacDonald et al. (1997) and Docherty (1998). Based on recent studies with gene-targeted and transgenic mice, .alpha..sub.2A-adrenocept- ors mediate most of the pharmacological actions ascribed to currently available .alpha..sub.2-adrenoceptor agonists, including inhibition of neurotransmitter release, central hypotensive and bradycardic effects, sedation and anesthesia, and analgesia. The same studies indicate that .alpha..sub.2B-adrenoceptors mediate peripheral pressor responses in response to agonist activation (Link et al. 1996, Macmillan et al. 1996) and thus play a significant role in the onset of hypertension (Calzada and Artinano 2001). Other physiological or pharmacological effects have not been associated with certainty with this receptor subtype. The .alpha..sub.2C-adrenoceptor subtype appears to be involved in regulation of complex behaviors. It is not known that this subtype would have important functions in peripheral tissues outside the central nervous system or in cardiovascular regulation. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method for diagnosing, monitoring and treating hypertension and other cardiac problems Inventor(s): Chio, Shiu-Shin ; (Rancho Santa Fe, CA) Correspondence: E. Victor Indiano, Esq.; Suite 850; One North Pennsylvania Street; Indianapolis; IN; 46204; US Patent Application Number: 20010016690 Date filed: December 15, 2000 Abstract: A method is disclosed for diagnosing, monitoring and treating cardiovascular pathologies. Among the hemodynamic parameters of interest are peripheral resistance, compliance, and cardiac (left ventricular) output. Peripheral resistance determined according to the present invention has been found to be a reliable indicator, not only of hypertension, but also of the cause of the hypertension. The determined peripheral resistance can be compared against a predetermined threshold value. This comparison helps to foster a diagnosis of a hypertensive condition. Excerpt(s): The present invention relates to a method for diagnosing, monitoring and treating cardiovascular pathologies, and more particularly to a method of determining
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hemodynamic parameters in a human cardiovascular system by analyzing arterial waveforms, methods for using the parameters so determined for diagnosing hypertension and other cardiovascular problems and diseases, and devices that incorporate the methods of the present invention... Cardiovascular disease is a leading cause of death and disability. One cardiovascular disease that affects a large number of people is hypertension, which is defined as abnormally elevated blood pressure. Hypertension is quite common. It is estimated that over 60,000,000 Americans suffer from hypertension... To prevent cardiac disorders from causing death, serious illness and disability, it is important to monitor the condition of a person's cardiovascular system, and to analyze the data from the monitoring so performed to determine whether any pathologies exist in the person's cardiovascular system that should be treated to prevent further degradation of the patient's cardiovascular system. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method for treatment of ocular hypertension and glaucoma Inventor(s): Ueno, Ryuji ; (Montgomery, MD), Ueno, Ryuji ; (Montgomery, MD) Correspondence: SUGHRUE MION, PLLC; 2100 Pennsylvania Avenue, NW; Washington; DC; 20037-3213; US, SUGHRUE MION, PLLC; 2100 Pennsylvania Avenue, NW; Washington; DC; 20037-3213; US Patent Application Number: 20030060511 Date filed: August 22, 2002 Abstract: Provided is a method for treating ocular hypertension and glaucoma, which comprises administrating an effective amount of 15-keto-prostaglandin compound having a ring structure at the end of the .omega. chain to the eyes of a mammalian subject in need of such treatment once a day. According to the method, single administration of the compound effectively lower the IOP of the subject throughout the day. Excerpt(s): The present invention relates to a method for treating ocular hypertension and glaucoma of a mammalian subject... The present invention relates to a method for treating ocular hypertension and glaucoma of a mammalian subject... Subscript 3: 5,6-, 13,14-, and 17,18-triunsaturated-15-OH... Subscript 3: 5,6-, 13,14-, and 17,18triunsaturated-15-OH... Further, the PGFs are classified, according to the configuration of the hydroxyl group at the 9-position, into .alpha. type (the hydroxyl group is of an .alpha.-configuration) and .beta. type (the hydroxyl group is of a .beta.-configuration)... Further, the PGFs are classified, according to the configuration of the hydroxyl group at the 9-position, into .alpha. type (the hydroxyl group is of an .alpha.-configuration) and .beta. type (the hydroxyl group is of a .beta.-configuration). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 313
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Method for treatment of ocular hypertension and glaucoma Inventor(s): Ueno, Ryuji ; (Montgomery, MD), Ueno, Ryuji ; (Montgomery, MD) Correspondence: SUGHRUE MION, PLLC; 2100 Pennsylvania Avenue, NW; Washington; DC; 20037-3213; US, SUGHRUE MION, PLLC; 2100 Pennsylvania Avenue, NW; Washington; DC; 20037-3213; US Patent Application Number: 20030060511 Date filed: August 22, 2002 Abstract: Provided is a method for treating ocular hypertension and glaucoma, which comprises administrating an effective amount of 15-keto-prostaglandin compound having a ring structure at the end of the .omega. chain to the eyes of a mammalian subject in need of such treatment once a day. According to the method, single administration of the compound effectively lower the IOP of the subject throughout the day. Excerpt(s): The present invention relates to a method for treating ocular hypertension and glaucoma of a mammalian subject... The present invention relates to a method for treating ocular hypertension and glaucoma of a mammalian subject... Subscript 3: 5,6-, 13,14-, and 17,18-triunsaturated-15-OH... Subscript 3: 5,6-, 13,14-, and 17,18triunsaturated-15-OH... Further, the PGFs are classified, according to the configuration of the hydroxyl group at the 9-position, into .alpha. type (the hydroxyl group is of an .alpha.-configuration) and .beta. type (the hydroxyl group is of a .beta.-configuration)... Further, the PGFs are classified, according to the configuration of the hydroxyl group at the 9-position, into .alpha. type (the hydroxyl group is of an .alpha.-configuration) and .beta. type (the hydroxyl group is of a .beta.-configuration). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of assaying modulators of hypertension Inventor(s): Ruiz-Opazo, Nelson ; (Westwood, MA) Correspondence: CLARK & ELBING LLP; 101 FEDERAL STREET; BOSTON; MA; 02110; US Patent Application Number: 20020095691 Date filed: January 7, 2002 Abstract: The invention features methods for assaying compounds that affect hypertension by using an animal model with a functionally variant hypertension susceptibility gene. Excerpt(s): The invention relates to methods useful for delaying or ameliorating diseases associated with hypertension... Essential hypertension (EHT; 1) is a paradigmatic, complex, and multifactorial condition. Genes that mediate EHT have therefore been difficult to isolate and characterize, requiring multiple lines of evidence to establish their roles in EHT pathogenesis... In view of the wide range of disorders that are associated with hypertension, it would be desirable to identify compounds for the treatment or prevention of hypertension. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of determining volume dependent hypertension via reduction in phosphorylation Inventor(s): Puschett, Jules B. ; (New Orleans, LA) Correspondence: Arnold B. Silverman; Eckert Seamans Cherin & Mellott, LLC; 44th Floor; 600 Grant Street; Pittsburgh; PA; 15219; US Patent Application Number: 20010044121 Date filed: June 22, 2001 Abstract: A method of determining the presence of chronic volume dependent hypertension is provided-wherein a determination is made as to whether there has been a substantial reduction in phosphorylation of the blood-derived protein or renal proximal brush border membrane protein and if such reduction exists concluding that chronic volume dependent hypertension exists in a patient. The method may advantageously be practiced by employing blood serum or blood plasma as the body specimen containing the protein in determining whether a patient has chronic volume dependent hypertension, a cellular component of the blood, such as a blood-derived protein coming from the plasma membrane of lymphocytes. The method may include subsequent therapeutic patient treatment. Related diagnostic apparatus is also provided. Excerpt(s): The present invention provides a means for determining whether a patient has volume dependent hypertension and, more specifically, it provides such a method based upon determining if a substantial reduction in phosphorylation of a specific protein exists. The invention also relates to a diagnostic apparatus employable in making such determination... Elevated blood pressure or hypertension has long been recognized as a health problem. It is a very common disease which can have widespread effects on a patient's body and frequently, unlike numerous other diseases, is asymptomatic... Despite known means of measuring blood pressure of a patient as by a sphygmomanometer, for example, there is lacking an accurate reliable means of detecting the presence of volume dependent hypertension involving higher arterial blood pressure by use of a body specimen, such as blood serum or blood plasma. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of diagnosing pulmonary hypertension Inventor(s): Trembath, Richard C. ; (Rutland, GB), Loyd, James E. ; (Nashville, TN), Thomson, Jennifer R. ; (Leeds, GB), Machado, Rajiv D. ; (Leicester, GB), Pauciulo, Michael W. ; (Blue Ash, OH), Foroud, Tatiana ; (Indianapolis, IN), Lane, Kirk B. ; (Brentwood, TN), Nichols, William C. ; (Loveland, OH), Phillips, John A. III ; (Brentwood, TN) Correspondence: NEEDLE & ROSENBERG, P.C.; The Candler Building, Suite 1200; 127 Peachtree Street, N.E.; Atlanta; GA; 30303-1811; US Patent Application Number: 20020102576 Date filed: July 17, 2001 Abstract: This invention relates generally to a method of identifying an individual having an increased susceptibility to developing Familial Primary Pulmonary Hypertension (FPPH), as well as to a method for diagnosing an individual suffering from FPPH. The invention also relates to a method of identifying an individual having an increased susceptibility to developing (non-familial) Primary Pulmonary
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Hypertension (PPH), as well as to a method for diagnosing an individual suffering from PPH. Excerpt(s): This application claims benefit of U.S. Provisional Application No. 60/218,740, filed Jul. 17, 2000, and U.S. Provisional Application No. 60/220,133, filed Jul. 21, 2000. Application Ser. No. 60/218,740, filed Jul. 17, 2000, and U.S. Provisional Application No. 60/220,133, filed Jul. 21, 2000, are hereby incorporated herein by reference... This invention relates generally to a method of identifying an individual having an increased susceptibility to developing Familial Primary Pulmonary Hypertension (FPPH), as well as to a method for diagnosing an individual suffering from FPPH. The invention also relates to a method of identifying an individual having an increased susceptibility to developing non-familial, or sporadic, Primary Pulmonary Hypertension (PPH), as well as to a method for diagnosing an individual suffering from sporadic PPH. The invention also relates to a method of identifying an agent capable of altering the symptoms of PPH in an individual suffering from familial or sporadic PPH, comprising contacting a test agent with Bone Morphogenic Protein Receptor II (BMPRII) and determining whether the test agent alters BMPR-II activity, wherein an alteration in BMPR-II activity in the presence of the test agent as compared with BMPR-II activity in the absence of the test agent indicates that the test agent is capable of altering the symptoms of PPH in an individual suffering from familial or sporadic PPH... Primary pulmonary hypertension (PH) is characterized by sustained elevation of pulmonary artery pressure (greater than 25 mmHg at rest and greater than 30 mmHg during exercise) and with no identifiable cause, such as recurrent thromboembolism, chronic hypoxic lung disease or left-sided cardiac disease. PPH is twice as common in females than males and symptoms develop typically in the 3.sup.rd and 4.sup.th decades of life, although the disease may occur at any age. Despite advances in therapy, mortality in PPH remains high with mean survival from onset of disease only 2.5 year. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method of treating isolated systolic hypertension Inventor(s): Ohlstein, Eliot H. ; (Glenmoore, PA), Brooks, David P. ; (West Chester, PA), Ruffolo, Robert R. JR. ; (Spring City, PA), Feuerstein, Giora Z. ; (Wynnewood, PA) Correspondence: GLAXOSMITHKLINE; Corporate Intellectual Property - UW2220; P.O. Box 1539; King of Prussia; PA; 19406-0939; US Patent Application Number: 20030045561 Date filed: September 19, 2002 Abstract: This invention relates to the use of eprosartan to treat isolated systolic hypertension. Excerpt(s): This invention relates to the use of eprosartan, which is (E)-.alpha.-[2-nbutyl-1-[(4-carboxyphenyl)methyl]-1H-imidazol-5-yl]methy- lene-2-thiophenepropionic acid monomethanesulfonate, to treat isolated systolic hypertension... The reninangiotensin system plays a major role in the long-term control of blood pressure. Inhibition of this system with ACE inhibitors, and more recently angiotensin II (AII) receptor antagonists, has provided important therapeutics for the treatment of hypertension. Additionally, it is known that the sympathetic nervous system plays an important role in blood pressure control. Indeed, sympathetic nervous system activity is a major determinant of systolic hypertension, which is now recognized as a significant risk factor for cardiovascular disease... The compound (E)-.alpha.-[2-n-butyl-1-[(4-
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carboxyphenyl)methyl]-1H-imidazol-5-yl]methylene-2-thiophenepropionic acid monomethanesulfonate is known by the name "eprosartan" and is the subject of U.S. Pat. No. 5,185,351 (the '351 patent), issued Feb. 9, 1993. This compound is a nonpeptide AII receptor antagonist. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method of treating portal hypertension Inventor(s): Rockey, Don C. ; (Chapel Hill, NC) Correspondence: NIXON & VANDERHYE P.C.; 1100 North Glebe Road, 8th Floor; Arlington; VA; 22201; US Patent Application Number: 20020006396 Date filed: March 14, 2001 Abstract: The present invention relates, in general, to portal hypertension and, in particular, to a method of reducing portal hypertension using an isoform of nitric oxide synthase. Excerpt(s): This application claims priority from U.S. Provisional Application No. 60/189,088, filed Mar. 14, 2000, the entire content of which is incorporated herein by reference... The present invention relates, in general, to portal hypertension and, in particular, to a method of reducing portal hypertension using an isoform of nitric oxide synthase (NOS)... The common result of many types of chronic liver injury is cirrhosis, which leads to increased intrahepatic resistance and portal hypertension (Friedman, N. Engl. J. Med. 328:1828-1835 (1993). Portal hypertension in turn has profound clinical consequences, many of which are associated with substantial morbidity and mortality. The pathologic basis of portal hypertension is complex and involves multiple factors (Shah et al, Hepatology 27(l):279-288 (1998)). However, in most instances an increase in intrahepatic resistance to blood flow is an early and critical component. Recent evidence links perisinusoidal stellate cells (also known as Ito cells or lipocytes), which are analogous to tissue pericytes or vascular smooth muscle cells, to a role in portal hypertension via their capacity to regulate blood flow within the liver by contraction and constriction of sinusoids (Bauer et al, Am. J. Physiol. 267:G143-G149 (1994), Zhang et al, Am. J. Physiol. 266:G624-G632 (1994), Bauer et al, Hepatology 22(5):1565-1576 (1995), Okumura et al, Hepatology 19:155-161 (1994), Suematsu et al, J. Clin. Invest. 96(5):2431-2437 (1995)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods and compositions for treating hypertension Inventor(s): Adams, Michael A. ; (Kingston, CA), Bridge, Suzanne K. ; (Oakville, CA) Correspondence: PARTEQ Innovations; Room 1625; Biosciences Complex; Queen's University; Kingston; ON; K7L 3N6; CA Patent Application Number: 20030087911 Date filed: August 16, 2001 Abstract: Methods are provided for preventing or inhibiting adverse cardiovascular effects associated with administration of a sympathetic nervous system antagonist in a subject, in which a subject in need thereof is administered a sympathetic nervous system
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antagonist and an endothelin antagonist. Methods of treating hypertension in a subject are also provided, in which a subject in need thereof is administered a sympathetic nervous system antagonist and an endothelin antagonist. Methods for improving the efficacy of a sympathetic nervous system antagonist are also provided, comprising administering to a subject in need thereof a sympathetic nervous system antagonist together with an endothelin antagonist. Methods of treating prostate cancer or benign prostate hyperplasia (BPH) in a subject are also provided, in which a subject in need thereof is administered a sympathetic nervous system antagonist and an endothelin antagonist. The sympathetic nervous system antagonist may be an alpha-adrenoceptor antagonist, a ganglionic blocking agent or another inhibitor of the actions of the sympathetic nervous system. Excerpt(s): This application claims the benefit of priority of U.S. Provisional Patent Application No. 60/226,098, filed 18 August 2000, the contents of which are incorporated herein by reference in their entirety... This invention relates to methods and compositions for treating hypertension, endothelial abnormalities or adverse effects induced by administration of sympathetic nervous system antagonists, using endothelin antagonists in combination with sympathetic nervous system antagonists... The interim analysis of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) has seriously challenged the concept that mean arterial pressure (MAP) lowering per se is an appropriate primary therapeutic endpoint. ALLHAT is an ongoing clinical trial involving more than 40,000 patients with hypertension and at least one other coronary heart disease (CHD) risk factor. It is a randomized, double-blind, activecontrolled trial to determine meaningful differences between 4 different antihypertensive agents: a diuretic, chlorthalidone; an .alpha..sub.1-adrenoceptor antagonist (one type of "alpha-blocker"), doxazosin; a calcium channel blocker, amlodipine; and an angiotensin converting enzyme (ACE) inhibitor, lisinopril. Recently the published interim report of approximately 24,000 patients by the ALLHAT Data and Safety Monitoring Board (DSMB) recommended discontinuation of one of the treatment arms that involved the .alpha..sub.1-adrenoceptor antagonist. The conclusions in the interim report stated that the alpha-blocker, when compared with the diuretic, was not effective in preventing cardiovascular end points i.e. it lacked equivalent impact on morbidity and mortality risks (ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group, JAMA 2000; 283(15): 1967-1975). Explicitly, the alphablocker arm of the study was terminated because patients had an overall 25% increase in the risk of cardiovascular events, including more than twice the risk of congestive heart failure (CHF) within the first two years of the study (ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group, JAMA 2000; 283(15): 1967-1975). These serious negative effects occurred despite the fact that the alphablocker had beneficial effects both on cholesterol and blood pressure control. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods and pharmaceutical formulations for the treatment of pulmonary hypertension and methods for screening compounds useful in the treatment of pulmonary hypertension Inventor(s): Schwarz, Margaret A. ; (La Canada-Flintridge, CA) Correspondence: MYERS BIGEL SIBLEY & SAJOVEC; PO BOX 37428; RALEIGH; NC; 27627; US Patent Application Number: 20030039652 Date filed: October 21, 2002 Abstract: A method of treating pulmonary hypertension in a subject in need of such treatment comprises inhibiting EMAP II activity in the subject by an amount effective to treat the pulmonary hypertension in the subject (e.g., in the lungs and more particularly in the pulmonary vasculature). Pharmaceutical formulations useful for carrying out such methods (e.g., an antibody that specifically binds to EMAP II in a pharmaceutically acceptable carrier) and screening techniques useful for identifying additional compounds that can be used for carrying out such methods are also disclosed. Excerpt(s): This application claims the benefit of U.S. Provisional Application Serial No. 60/177,008, filed Jan. 19, 2000 and U.S. Provisional Application Serial No. 60/197,492, filed Apr. 17, 2000, the disclosures of both of which are incorporated by reference herein in their entirety... This invention relates to pulmonary hypertension and compounds, formulations and methods useful in the treatment thereof... Pulmonary hypertension (PHTN) is a serious disorder characterized by an increase in pulmonary vascular resistance and classified clinically as either primary pulmonary hypertension or secondary pulmonary hypertension. In its most common form, pulmonary hypertension usually presents as a manifestation of an obvious or explicable increase in vascular resistance, such as obstruction to blood flow by pulmonary emboli, malfunction of the heart's valves or muscle in handling blood after its passage through the lungs, diminution in pulmonary vessel diameter as a reflex response to hypoventilation and/or low oxygenation, or a mismatch of vascular capacity and essential blood flow, such as shunting of blood in congenital abnormalities or surgical removal of lung tissue. Such pulmonary hypertension is referred to as secondary pulmonary hypertension. Secondary pulmonary hypertension may be a result of chronic obstructive or interstitial lung disease, recurrent pulmonary emboli, liver disease, or pre-existing heart disease. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods for treating hypertension and angina using salts of optically pure (-) amplodipine Inventor(s): Young, James W. ; (Palo Alto, CA) Correspondence: PENNIE AND EDMONDS; 1155 AVENUE OF THE AMERICAS; NEW YORK; NY; 100362711 Patent Application Number: 20010029260 Date filed: April 24, 2001 Abstract: Methods and compositions are disclosed utilizing the optically pure (-) isomer of amlodipine. This compound is a potent drug for the treatment of hypertension while avoiding the concomitant liability of adverse effects associated with the racemic mixture of amlodipine. The (-) isomer of amlodipine is also useful for the treatment of angina
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and such other conditions as may be related to the activity of (-) amlodipine as a calcium channel antagonist such as cerebral ischemia, cerebral disorders, arrhythmias, cardiac hypertrophy, coronary vasospasm, myocardial infarction, renal impairment and acute renal failure, without the concomitant liability of adverse effects associated with the racemic mixture of amlodipine. Excerpt(s): This invention relates to novel compositions of matter containing optically pure (-) amlodipine. These compositions possess potent activity in treating both systolic and diastolic hypertension while avoiding adverse effects including but not limited to edema of the extremities, headache and dizziness, which are associated with administration of the racemic mixture of amlodipine. Additionally, these novel compositions of matter containing optically pure (-) amlodipine are useful in treating angina and such other conditions as may be related to the activity of (-) amlodipine as a calcium channel antagonist including but not limited to cerebral ischemia, cerebral disorders, arrhythmias, cardiac hypertrophy, coronary vasospasm, myocardial infarction, renal impairment and acute renal failure--while avoiding the adverse effects associated with administration of the racemic mixture of amlodipine. Also disclosed are methods for treating the above-described conditions in a human while avoiding the adverse effects that are associated with the racemic mixture of amlodipine, by administering the (-) isomer of amlodipine to said human... Many organic compounds exist in optically active forms, i.e., they have the ability to rotate the plane of planepolarized light. In describing an optically active compound, the prefixes D and L or R and S are used to denote the absolute configuration of the molecule about its chiral center(s). The prefixes d and l or (+) and (-) are employed to designate the sign of rotation of plane-polarized light by the compound, with (-) or 1 meaning that the compound is levorotatory. A compound prefixed with (+) or d is dextrorotatory. For a given chemical structure, these compounds, called stereoisomers, are identical except that they are mirror images of one another. A specific stereoisomer may also be referred to as an enantiomer, and a mixture of such isomers is often called an enantiomeric or racemic mixture... Stereochemical purity is of importance in the field of pharmaceuticals, where 12 of the 20 most prescribed drugs exhibit chirality. A case in point is provided by the L-form of the .beta.-adrenergic blocking agent, propranolol, which is known to be 100 times more potent than the D-enantiomer. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods for treatment and prevention of disorders resulting from hypertension of neck and shoulder muscles Inventor(s): Krullaards, Robert Leonard ; (Leidschendam, NL) Correspondence: TOWNSEND AND TOWNSEND AND CREW, LLP; TWO EMBARCADERO CENTER; EIGHTH FLOOR; SAN FRANCISCO; CA; 94111-3834; US Patent Application Number: 20030149379 Date filed: October 9, 2002 Abstract: Methods for treatment and prevention of disorders resulting from hypertension of neck and shoulder muscles, in particular hypertension of the scalenius muscles, comprise administering a training regime to a subject suffering from the disorders, whereby the training regime comprises manipulating an object while maintaining a pinch-grip force exerted by the fingers on the object below a given threshold value. The object preferably has a pressure sensor that generates a signal
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when the pinch-grip force exceeds the threshold value. The object may be a writing instrument whereby the training may comprise writing exercises. Excerpt(s): This application is a continuation-in-part of application Ser. No. 10/168,725, (Attorney Docket No. 89988-000000), filed on Jun. 21, 2002, corresponding to the National Phase of PCT/NL00/00957, filed Dec. 22, 2000, which claimed the benefit of the Netherlands Patent No. NL 1013921, filed on Dec. 22, 1999, the full disclosures of which are incorporated herein by reference... The present invention relates to methods for treatment and prevention of disorders resulting from hypertension of neck and shoulder muscles, in particular hypertension of the scalenius muscles. The method comprises administering a training regime to a subject suffering from the disorders, whereby the training regime comprises manipulating an object while maintaining the pinch-grip force exerted by the fingers on the object below a given threshold value. The object preferably has a pressure sensor that generates a signal when the pinch-grip force exceeds the threshold value... In recent times many problems have arisen in relation to the results of tensions prevailing in human muscles. "RSI" in particular has received much media attention in recent times. The problem of "tennis elbow" has however been known for much longer. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods of modulating symptoms of hypertension Inventor(s): Aiello, Lloyd P. ; (Cambridge, MA) Correspondence: LOUIS MYERS; Fish & Richardson P.C.; 225 Franklin Street; Boston; MA; 02110-2804; US Patent Application Number: 20020091082 Date filed: September 13, 2001 Abstract: The invention features methods of treating hypertension and related disorders and conditions, e.g., diabetic retinopathy, by inhibiting VEGF-KDR signaling pathway components, e.g., PKC-zeta and/or PI3 kinase 1. Excerpt(s): This application claims the benefit of U.S. Provisional Application Serial No. 60/232,503, filed Sep. 13, 2000, which is incorporated herein by reference in its entirety... Concomitant hypertension exacerbates a wide variety of disease including ocular disorders such as diabetic retinopathy, age related macular degeneration, retinal vein inclusion, and retinal macro aneurysms. In addition, hypertension itself causes a significant retinopathy as well as alterations throughout the body including increased risk of cardiovascular disease, myocardial infraction, stroke and death. The mechanisms by which hypertension exacerbates these assorted disorders are not well understood... Numerous vision-threatening diseases such as diabetic retinopathy are exacerbated by coexistent hypertension. Epidemiological studies identify hypertension as an independent risk factor for diabetic retinopathy. Patients with higher ranges of blood pressure are up to three times more likely to develop PDR diabetic retinopathy (Roy (2000) Arch. Ophthalmol. 118: 105-115), 35% more likely to have retinopathy progression, 47% more likely to have visual loss (UK Prospective Diabetes Study Group. (1998) British Medical Journal 317: 703-713) and three times more likely to develop diffuse macular edema (Lopes et al. (1999) Acta Ophthalmol Scand. 77: 170-175). The sight threatening complications of diabetic retinopathy are characterized by development of retinal neovascularization and/or retinal vascular permeability. Severe
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hypertension itself can induce a retinopathy characterized by increased retinal vascular leakage. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods of treating hypertension and compositions for use therein Inventor(s): Schreiner, George F. ; (Los Altos Hills, CA), Johnson, Richard J. ; (Seattle, WA) Correspondence: KNOBBE MARTENS OLSON & BEAR LLP; 2040 MAIN STREET; FOURTEENTH FLOOR; IRVINE; CA; 92614; US Patent Application Number: 20020193288 Date filed: February 26, 2002 Abstract: The present invention provides methods and compositions for treating hypertension. The methods generally involve administering a factor which increases angiogenesis and/or vascular permeability. Compositions for use in the methods are also provided. Excerpt(s): This is a continuation of U.S. patent application Ser. No. 09/392,932 filed on Sep. 9, 1999, which claims priority to provisional application Serial No. 60/099,694 filed on Sep. 9, 1998, provisional application Serial No. 60/126,406 filed Mar. 26, 1999, and provisional application Serial No. 60/126,615 filed Mar. 27, 1999, all disclosures are hereby incorporated by reference... The present invention relates to methods for treating hypertension, using a factor that stimulates angiogenesis and/or promotes vascular permeability... Systemic hypertension is the most prevalent cardiovascular disorder in the United States, affecting over 60 million Americans. In spite of increasing public awareness and a rapidly expanding array of anti-hypertensive medications, hypertension remains one of the leading causes of cardiovascular morbidity and mortality. Hypertension treatments have focused on stimulating the relaxation of the peripheral vasculature (vasodilation), depressing cardiac function, or by stimulating salt transport by blocking epithelial transport of sodium or chloride (diuresis). "Textbook of Medical Physiology", Guyton and Hall, eds. p. 234 (1996) W. B. Saunders. In addition, adverse metabolic effects have been observed with treatment using certain classes of antihypertensive treatment in coronary disease prevention. "Cecil Textbook of Medicine"pp. 252-269 (1992) W. B. Saunders. Therefore, there is a need to develop improved methods of treatment of hypertension. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Ophthalmic compositions for treating ocular hypertension Inventor(s): Ponticello, Gerald S. ; (Lansdale, PA), Sugrue, Michael F. ; (Blue Bell, PA) Correspondence: Merck & Co., Inc.; Patent Department; P.O. Box 2000 - RY60-30; Rahway; NJ; 07065-0907; US Patent Application Number: 20020094981 Date filed: December 17, 2001 Abstract: Combinations of a prostaglandin or an opthalmologically acceptable salt thereof and a topical carbonic anhydrase inhibitor or an opthalmologically acceptable salt thereof are particularly useful in the treatment of ocular hypertension and
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glaucoma. The combinations are characterized by an improved effect and reduced sideeffects. Excerpt(s): This is a continuation of Merck & Co., Inc., attorney docket number 19979 (U.S. Ser. No. 09/086,829) filed May 29, 1998, which was provisionally filed May 30, 1997 as U.S. Ser. No. 60/048,140... Glaucoma is a degenerative disease of the eye wherein the intraocular pressure is too high to permit normal eye function. As a result, damage may occur to the optic nerve head and result in irreversible loss of visual function. If untreated, glaucoma may eventually lead to blindness. Ocular hypertension, i.e., the condition of elevated intraocular pressure without optic nerve head damage or characteristic glaucomatous visual field defects, is now believed by the majority of ophthalmologists to represent merely the earliest phase in the onset of glaucoma... Many of the drugs formerly used to treat glaucoma proved not entirely satisfactory. The early methods of treatment of glaucoma employing pilocarpine produced undesirable local effects that made this drug, though valuable, unsatisfactory as a first line drug. More recently, clinicians have noted that many .beta.-adrenergic antagonists are effective in reducing intraocular pressure. While many of these agents are effective for this purpose, there exist some patients with whom this treatment is not effective or not sufficiently effective. Many of these agents also have other characteristics, e.g., membrane stabilizing activity, that become more apparent with increased doses and render them unacceptable for chronic ocular use. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Pharmaceutical compositions and method for the treatment of hypertension Inventor(s): Waldeck, Harald ; (Isernhagen, DE), Thormaehlen, Dirk ; (Rheden, DE), Wilkins, Martin R. ; (Buckinghamshire, GB) Correspondence: CROWELL & MORING LLP; INTELLECTUAL PROPERTY GROUP; P.O. BOX 14300; WASHINGTON; DC; 20044-4300; US Patent Application Number: 20020052361 Date filed: August 16, 2001 Abstract: The present invention relates to the use of benzazepine-N-acetic acid derivatives which contain an oxo-group in the .alpha.-position to the nitrogen atom and are substituted in position 3 by a 1-(carboxyalkyl)cyclo-entylcarbonylamino radical, and their salts and biolabile esters for the treatment of hypertension, particularly for the treatment of certain forms of secondary hypertension, in larger mammals and particularly humans, and for the production of pharmaceutical compositions suitable for this treatment. The cause of the hypertension to be treated may have a wide variety of origins. The invention particularly relates to the treatment of those forms of secondary hypertension which may occur as a result of various non-cardiac diseases. Excerpt(s): This application is a continuation of International Patent Application No. PCT/EP00/01068, filed Feb. 10, 2000, designating the Unites States of America, the entire text of which is incorporated herein by reference. Convention priority is also claimed based on Federal Republic of Germany patent application no. DE 199 06 310.9, filed Feb. 16, 1999... The present invention relates to the use of benzazepine-N-acetic acid derivatives which contain an oxo-group in the .alpha.-position to the nitrogen atom and are substituted in position 3 by a 1-(carboxyalkyl)cyclo-pentylcarbonylamino radical, and their salts and biolabile esters for the treatment of hypertension, particularly of certain forms of secondary hypertension, in larger mammals and particularly
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humans, and for the production of pharmaceutical compositions suitable for this treatment. The cause of the hypertension to be treated can have a wide variety of origins. In particular, the invention relates to the treatment of those forms of secondary hypertension which may occur as a result of various non-cardiac diseases... Benzazepine-N-acetic acid derivatives which contain an oxo group in .alpha.-position to the nitrogen atom and are substituted in position 3 by a 1-(carboxyalkyl)cyclopentylcarbonylamino radical, and their salts and biolabile esters fall under the scope of protection of the benzazepine, benzoxazepine and benzothiazepine-N-acetic acid derivatives which contain an oxo group in the .alpha.-position to the nitrogen atom and are substituted in position 3 by a 1-(carboxyalkyl)cyclopentyl-carbon- ylamino radical and have NEP-inhibitory effects on the heart, as described in Waldeck et al., U.S. Pat. No. 5,677,297 (=DE 195 10 566). The benzazepine-N-acetic acid compounds used in the present invention can be produced by the methods described in said U.S. Pat. No. 5,677,297. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Pleurotus extract and use in treating hypertension Inventor(s): Wang, Rui ; (Saskatoon, CA), Huang, Yaoge ; (Saskatoon, CA), Zhao, Weimin ; (Nepean, CA) Correspondence: GREENLEE WINNER AND SULLIVAN P C; 5370 MANHATTAN CIRCLE; SUITE 201; BOULDER; CO; 80303; US Patent Application Number: 20030161842 Date filed: December 20, 2002 Abstract: The invention provides an extract of the Pleurotus genus such as Pleurotus eryngii (DC. et Fr) Qul to prevent and treat hypertension, and enhance cardiovascular health. Further, the invention provides pharmaceutical compositions containing the extract as an active ingredient, in a pharmaceutically or therapeutically acceptable carrier. The invention also provides a method of preventing and treating hypertension by administration of the extract. Further, there is provided a method for preparing the extract and evaluating the extract using in vitro or in vivo tests to ensure antihypertensive activity. Excerpt(s): This application claims priority from U.S. Provisional Patent Application No. 60/341,209 filed Dec. 20, 2001, which is incorporated by reference herein to the extent that there is no inconsistency with the present disclosure... The present invention relates to a mushroom extract prepared from the genus Pleurotus such as Pleurotus eryngii (DC. et Fr.) Qul. and its preparation and use in the prevention and treatment of hypertension, and enhancement of cardiovascular health... Hypertension is a disorder characterized by persistently high arterial blood pressure, whereby the systolic blood pressure (representing the pressure generated when the heart beats) remains consistently higher than 140 mm Hg, or diastolic blood pressure (representing the pressure in the vessels when the heart is at rest) remains consistently over 90 mm Hg. Hypertension can lead to stroke, heart attack or failure, cardiac arrhythmia, arteriosclerosis, or renal failure. Hypertension may have no known cause ("primary hypertension" or "essential hypertension") or be associated with other primary diseases ("secondary hypertension"). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Polymorphisms associated with hypertension Inventor(s): Fan, Jian Bing ; (Palo Alto, CA), Halushka, Marc Kenneth ; (Cleveland Heights, OH), Chakravarti, Aravinda ; (Shaker Heights, OH) Correspondence: TOWNSEND AND TOWNSEND AND CREW LLP; TWO EMBARCADERO CENTER; 8TH FLOOR; SAN FRANCISCO; CA; 94111-3834; US Patent Application Number: 20030170699 Date filed: January 2, 2003 Abstract: The invention discloses a collection of polymorphic sites in genes know or suspected to have a role in hypertension. The invention provides nucleic acids including such polymorphic sites. The nucleic acids can be used as probes or primers or for expressing variant proteins. The invention also provide methods of analyzing the polymorphic forms occupying the polymorphic sites. Excerpt(s): This application derives priority from U.S. Ser. No. 60/084,641 filed May 7, 1998, which is incorporated by reference in its entirety for all purposes... Hypertension, or high blood pressure, is a common disease affecting 50 million Americans and contributing to over 200,000 deaths annually from stroke, myocardial infarction, and end-stage renal disease. The disease is multifactorial and numerous genetic and nongenetic components, such as salt intake, age, diet, and body mass, are suspected to contribute. A specific cause of hypertension can typically be identified in only a small percentage of patients. Other patients with abnormally high blood pressure of unknown cause are said to have essential hypertension... The existence of a genetic component to hypertension is known from twin studies, which have revealed a greater concordance of blood pressure in monozygotic twins that in dizygotic twins. Similarly, biological siblings have show greater concordance of blood pressure than adoptive siblings raised in the same household. Such studies have suggested that up to about 40% of the variations in blood pressure in the population are genetically determined. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Preventive, alleviative or remedy for hypertension Inventor(s): Mitsui, Yuki ; (Tokyo, JP), Suzuki, Atsushi ; (Tochigi, JP), Takahashi, Hirokazu ; (Tokyo, JP), Watanabe, Takuya ; (Tokyo, JP), Okawa, Wataru ; (Tokyo, JP), Eguchi, Yasuteru ; (Tokyo, JP) Correspondence: OBLON SPIVAK MCCLELLAND MAIER & NEUSTADT PC; FOURTH FLOOR; 1755 JEFFERSON DAVIS HIGHWAY; ARLINGTON; VA; 22202; US Patent Application Number: 20020192317 Date filed: July 11, 2002 Abstract: Provided is a preventive, ameliorant or remedy for hypertension excellent in both blood pressure lowering action and blood pressure-rise suppressing action and having high safety.This preventive, ameliorant or remedy for hypertension comprises a coffee bean extract. Excerpt(s): The present invention relates to a preventive, alleviative or remedy for hypertension which has excellent blood pressure lowering effects, blood-pressure-rise suppressing effects and safety and is available in the form of a food or pharmaceutical... Examples of a pharmaceutical used for treatment of hypertension include various neuroleptics acting on the neural-factor-related regulator system, ACE inhibitors acting
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on the heurohumoral-factor-relate- d regulator system, AT receptor antagonists, Ca antagonists acting on the vascular-endothelium-derived-substance-related regulator system, and hypotensive diuretics acting on the body-fluid-regulator system in the kidney. These pharmaceuticals are mainly used in medical institutions for patients suffering from severe hypertension... Under the present state, however, pharmaceuticals used as a measure against hypertension are a serious burden for patients because in spite of satisfactory effectiveness, their side effects are not a few. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Preventives and remedies for pulmonary hypertension Inventor(s): Inada, Yoshiyuki ; (Hyogo, JP), Yonemitsu, Yoshikazu ; (Fukuoka, JP), Ikeda, Yasuhiro ; (Fukuoka, JP), Sueishi, Katsuo ; (Fukuoka, JP), Egashira, Kensuke ; (Fukuoka, JP) Correspondence: TAKEDA PHARMACEUTICALS NORTH AMERICA, INC; INTELLECTUAL PROPERTY DEPARTMENT; 475 HALF DAY ROAD; SUITE 500; LINCOLNSHIRE; IL; 60069; US Patent Application Number: 20030162737 Date filed: March 22, 2003 Abstract: The present invention provides a prophylactic and/or therapeutic agent for pulmonary hypertension, comprising an antagonistic mutein of MCP-1 or a salt thereof, a DNA molecule comprising a nucleotide sequence encoding the antagonistic mutein of MCP-1, or a neutralizing antibody against MCP-1.The antagonistic mutein of MCP-1 or a salt thereof, the DNA molecule having a nucleotide sequence encoding the antagonistic mutein of MCP-1, or the neutralizing antibody against MCP-1 has hypotensive activity, and thus is useful as a pharmaceutical agent for preventing and/or treating pulmonary hypertension (primary pulmonary hypertension, in particular). Excerpt(s): The present invention relates to novel prophylactic and/or therapeutic agents for pulmonary hypertension... MPC-1 (Monocyte chemoattractant protein-1: macrophage chemotactic factor) is a member of the C--C chemokine family and is known to be highly expressed in the arteriosclerotic (e.g. atherosclerotic) lesion (Takeya, M. et al., Hum. Pathol. 24: 534-539 (1993); Yla-Herttuala, S. et al., Proc. Natl. Acad. Sci. USA, 88: 5252-5257 (1991))... On the other hand, primary pulmonary hypertension (PH) is a disease with poor prognosis, and heart-lung transplantation is the only therapy for this disease at present. However, heart-lung transplantation has considerable difficulty being used as a practical treatment due to the limited supply of donors. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Product comprising a heterotrimeric g protein signal transduction inhibitor associated with anti-hypertensive agent for therapeutic use in the treatment of arterial hypertension Inventor(s): Prevost, Gregoire ; (Antony, FR), Teillot, Marc ; (Paris, FR) Correspondence: BIERMAN MUSERLIAN AND LUCAS; 600 THIRD AVENUE; NEW YORK; NY; 10016 Patent Application Number: 20030004168 Date filed: July 3, 2002 Abstract: The invention concerns a product comprising at least an inhibitor of heterotrimeric G protein signal transduction, associated with at least another antihypertensive agent, in particular calcium channel blockers and conversion enzyme inhibitors, for simultaneous, separate or prolonged therapeutic use, in the treatment of hypertension. Excerpt(s): The present invention relates to a product comprising at least one G protein inhibitor, and preferably a compound of general formula (I) defined below, combined with at least one anti-hypertensive agent, preferably chosen from the group comprising calcium channel antagonists or conversion enzyme inhibitors, for simultaneous, separate or spread over time therapeutic use, in the treatment of arterial hypertension... Arterial hypertension is a very common disease and one to which a high morbidity and mortality rate is associated. According to age, treatment of hypertension must be considered when the systolic arterial pressure is higher than 160-180 mm of mercury and the diastolic pressure higher than 100-110 mm of mercury... The optimum strategy for the care of patients suffereing from hypertension is still under discussion. Nonpharmacological treatment (reduction of sodium intake in food, loss of weight, physical exercise, giving up tobacco products etc.) is a possibility in patients with moderate hypertension. Pharmacological treatment begins with monotherapy, which allows satisfactory blood pressure control in 50-60% of patients. Changing therapeutic class as well as combination with another class of anti-hypertensive agents represent the alternative treatments in the event of resistance to the first therapy (Beaufils and Element, Drugs, 56, 11-21, (1998)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Prostaglandin derivatives for the treatment of glaucoma or ocular hypertension Inventor(s): Resul, Bahram ; (Uppsala, SE), Stjernschantz, Johan Wilhelm ; (Uppsala, SE) Correspondence: KENYON & KENYON; ONE BROADWAY; NEW YORK; NY; 10004; US Patent Application Number: 20030181493 Date filed: December 27, 2002 Abstract: The invention relates to ophthalmological compositions for topical treatment of glaucoma or ocular hypertension comprising an effective intraocular pressure reducing amount of a prostaglandin derivative of PGA, PGB, PGD, PGE or PGF, in which the omega chain contains a ring structure, in an ophthalmologically compatible carrier. The invention further relates to the preparation of said compositions and their use for treatment of glaucoma or ocular hypertension.
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Excerpt(s): The invention is concerned with the use of prostaglandin derivatives of PGA, PGB, PGD, PGE and PGF, in which the omega chain has been modified with the common feature of containing a ring structure, for the treatment of glaucoma or ocular hypertension. The invention relates also to ophthalmic compositions, containing an active amount of these prostaglandin derivatives, and the manufacture of such compositions... Glaucoma is an eye disorder characterized by increased intraocular pressure, excavation of the optic nerve head and gradual loss of the visual field. An abnormally high intraocular pressure is commonly known to be detrimental to the eye, and there are clear indications that, in glaucoma patients, this probably is the most important factor causing degenerative changes in the retina. The pathophysiological mechanism of open angle glaucoma is, however, still unknown. Unless treated successfully glaucoma will lead to blindness sooner or later, its course towards that stage is typically slow with progressive loss of the vision... where P.sub.e is the episcleral venous pressure, generally regarded as being around 9 mm Hg, F the flow of aqueous humor, and R the resistance to outflow of aqueous humor through the trabecular meshwork and adjacent tissue into Schlemm's canal. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Role of PPH1 gene in pulmonary hypertension Inventor(s): Knowles, James A. ; (Rowaytn, CT), Morse, Jane H. ; (Bronx, NY) Correspondence: John P. White; Cooper & Dunham LLP; 1185 Avenue of the Americas; New York; NY; 10036; US Patent Application Number: 20020022229 Date filed: July 12, 2001 Abstract: This invention provides a method of detecting whether a subject is either predisposed to or afflicted with a pulmonary disease which comprises (1) obtaining a suitable sample from the subject; (2) detecting in the sample a bone morphogenetic protein receptor-II mutation which is not present in wildtype bone morphogenetic protein receptor-II, wherein the presence of a mutation indicates that the subject is predisposed to or afflicted with the pulmonary disease. In one embodiment, the pulmonary disease is Familial Primary Pulmonary Hypertension. Excerpt(s): This application is a continuation-in-part and claims the benefit of U.S. Provisional Application No. 60/217,773, filed Jul. 12, 2000, the contents of which are hereby incorporated by reference into this application... The invention disclosed herein was made with Government support under NIH Grant No. HL60056-02 from the National Heart, Lung and Blood Institute. Accordingly, the government has certain rights in this invention... Throughout this application, various publications are referenced within parentheses. Disclosures of these publications in their entireties are hereby incorporated by reference into this application to more fully describe the state of the art to which this invention pertains. Full bibliographic citations for these references may be found immediately preceding the claims. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Topical treatment of ocular hypertension, glaucoma, ischemic retinopathy and agerelated macular degeneration with ophthalmic formulation of dopamine antagonists Inventor(s): Chiou, George C.Y. ; (College Station, TX) Correspondence: MORRISON & FOERSTER LLP; 755 PAGE MILL RD; PALO ALTO; CA; 94304-1018; US Patent Application Number: 20030069232 Date filed: February 28, 2001 Abstract: This invention provides ocular formulations comprising an ocular drug and a carboxylic acid in an amount sufficient to maintain the pH of the formulation from about 4.5 to about 7.5. The ocular drug may be a dopamine antagonist and the acid may be lactic acid, citric acid or tartaric acid. In some aspects, the pH of the formulation is about 5.5 The ocular formulations of this invention provide enhanced bioavailability which results in increased drug concentrations across the cornea and in the eye ball, i.e., aqueous humor and intraocular organs and chambers. Moreover, the present formulations are non-irritating when applied topically and have a shelf-life of at least fourteen days at 25.degree. C. Methods are also provided to increase ocular blood flow by using present ocular formulations comprising dopamine antagonists or other drugs for the prevention and treatment of ocular hypertension, glaucoma, ischemic retinopathy and age-related macular degeneration (AMD). Excerpt(s): The present invention relates generally to ocular formulations and methods for using those formulations to improve blood flow to the retina and choroid to halt or reverse the course of visual deterioration. Accordingly, this invention transcends the related disciplines of pharmaceutical sciences, ocular pharmacology and medicine... Several potential drugs have been developed with high anticipation of treating various eye diseases, yet only a few of those potential drugs have reached the clinics because of the problems of drug delivery. Ocular drug delivery faces three major difficulties: first, the ocular bioavailability of the drug is often poor because the drug needs to cross the cornea to enter the eye ball, i.e., the aqueous humor and other interior anatomical organs of the eye; second, very often, the drug formulation is irritable when applied topically to the eye; and third, the ocular formulations are very unstable, i.e., have a short shelf-life, in the order of a few days to few weeks. For example, most, if not all dopamine antagonists do not dissolve in plain aqueous medium and, as a result, their non-aqueous formulations often produce severe eye irritation. Various absorption enhancers and antiirritants have been proposed in the prior art to overcome these difficulties. However, the search for a successful resolution to the problem continues... Accordingly, there is a need for stable ocular formulations that enhance the ocular bioavailability of a drug with reduced ocular irritation when administered topically. As the following description illustrates, the present invention meets this need. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Treatment of pulmonary hypertension Inventor(s): Ghazzi, Maha ; (Ann Arbor, MI), Pressler, Milton Lethan ; (Saline, MI) Correspondence: Charles W. Ashbrook; Warner-Lambert Company; 2800 Plymouth Road; Ann Arbor; MI; 48105; US Patent Application Number: 20020128259 Date filed: October 3, 2001
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Abstract: Disclosed is a method for treating pulmonary hypertension using a vasopressin antagonist. Excerpt(s): This invention relates to vasopressin antagonists for use in treating pulmonary hypertension. Specifically, this invention relates to the use of conivaptan for treating pulmonary hypertension... Pulmonary hypertension (PH) is a condition of increased pulmonary vascular resistance and pulmonary arterial pressure which interferes with ventilation-perfusion relationships. PH typically is characterized by increased blood pressure (above 30 mm Hg systolic and 12 mm Hg diastolic) within the pulmonary circulation. There are two subsets of pulmonary hypertension: primary (idiopathic or "unexplained") and secondary. The secondary form is by far the more prevalent. The most common causes of secondary pulmonary hypertension are heart disease and lung disease. Regardless of the root cause of the pulmonary hypertension, the resistance (precapillary) vessels of the lungs undergo anatomic change that contributes to the progression of pulmonary hypertension. Pulmonary arterial hypertension secondary to acquired heart disease begins with a disorder of the left ventricle that leads to pulmonary venous hypertension followed by pulmonary arterial hypertension... Arginine vasopressin, also known as antidiuretic hormone (ADH), is synthesized in the magnocellular neurosecretory cells of the paraventricular and supraoptic nuclei of the hypothalamus and stored in the posterior pituitary. There are 2 classes of AVP receptors, V.sub.1 and V.sub.2. There are 2 subclasses of V.sub.1 receptors, namely V.sub.1A and V.sub.1B. V.sub.1A receptors are found in the vasculature, and mediate the pressor response of AVP by increasing the contraction of blood vessels. Recent in vitro studies in the rat suggest that the lung contains the V.sub.1A receptor subtype. V.sub.1A receptors are also found on platelets, where they mediate platelet aggregation. V.sub.1B receptors are located in the anterior pituitary and mediate adrenocorticotropic hormone (ACTH) release. V.sub.2 receptors are located in the collecting ducts of the kidney; they are coupled to aquaporine channels and modulate free water clearance. Arginine vasopressin is released into the circulation in response to an increase in plasma osmolality (mediated by osmoreceptors) or a decrease in plasma volume or blood pressure (mediated by baroreceptors). However, there are other stimuli for AVP release, including norepinephrine, angiotensin II, emotion, nausea and vomiting, and fever. Elevated levels of AVP have been reported in patients with cardiac failure, although its pathophysiologic role is unknown. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Use of cloprostenol and fluprostenol analogues to treat glaucoma and ocular hypertension Inventor(s): May, Jesse A. ; (Fort Worth, TX), Desantis, Louis JR. ; (Fort Worth, TX), Dean, Thomas R. ; (Weatherford, TX), Sallee, Verney L. ; (Burleson, TX) Correspondence: ALCON RESEARCH, LTD.; R&D COUNSEL, Q-148; 6201 SOUTH FREEWAY; FORT WORTH; TX; 76134-2099; US Patent Application Number: 20020111381 Date filed: February 5, 2002 Abstract: Disclosed is the use of cloprostenol and fluprostenol analogues in combination with carbonic anhydrase inhibitors for the treatment of glaucoma and ocular hypertension and ophthalmic compositions therefor.
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Excerpt(s): The present application is a continuation of U.S. patent application Ser. No. 09/777,409, filed Feb. 6, 2001, now U.S. Pat. No. 6,344,478, which is a continuation of U.S. patent application Ser. No. 09/281,043, filed Mar. 30, 1999, now U.S. Pat. No. 6,184,250, which is a continuation-in-part of U.S. patent application Ser. No. 08/917,795, filed Aug. 21, 1997, now U.S. Pat. No. 5,889,052, which is a continuation of U.S. patent application Ser. No. 08/769,293, filed Dec. 18, 1996, now U.S. Pat. No. 5,665,773, which is a continuation of U.S. patent application Ser. No. 08/280,681, filed Jul. 26, 1994, now abandoned, which is a continuation-in-part of U.S. patent application Ser. No. 08/101,598 filed Aug. 3, 1993, now U.S. Pat. No. 5,510,383... The present invention relates to the treatment of glaucoma and ocular hypertension. In particular, the present invention relates to the use of cloprostenol and fluprostenol analogues for the treatment of glaucoma and ocular hypertension... The chemical name for cloprostenol is 16-(3chlorophenoxy)-17,18,19- ,20-tetranor PGF.sub.2.alpha.. Monograph No. 2397 (page 375) of The Merck Index, 11th Edition (1989) is incorporated herein by reference to the extent that it describes the preparation and known pharmacological profiles of cloprostenol. Fluprostenol has 15 the chemical name 16-(3-trifluoromethylphenoxy)-17,18,19,20tetranor PGF.sub.2.alpha.. Monograph No. 4121 (pages 656-657) of The Merck Index, 11th Edition (1989) is incorporated herein by reference to the extent that it describes the preparation and known pharmacological profiles of fluprostenol. Cloprostenol and fluprostenol are 16-aryloxy PGs and, in addition to the substituted aromatic ring, differ from the natural product PGF.sub.2.alpha. in that an oxygen atom is embedded within the lower (omega) chain. This oxygen interruption forms an ether functionality. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Use of DPPIV inhibitors as diuretic and anti-hypertensive agents Inventor(s): Knauf, Felix ; (Berlin, DE), Girardi, Adriana ; (S?atilde;o Paulo, BR), Aronson, Peter S. ; (Guilford, CT) Correspondence: MARY M. KRINSKY, Ph. D., J.D.; PATENT ATTORNEY; 79 TRUMBULL STREET; NEW HAVEN; CT; 06511; US Patent Application Number: 20020037829 Date filed: August 23, 2001 Abstract: Dipeptidyl peptidase IV inhibitors are used as diuretics and anti-hypertensive agents. Excerpt(s): This application claims priority benefit of provisional application U.S. Ser. No. 60/227,400, filed Aug. 23, 2000... This invention relates to a new class of diuretics and antihypertensive agents and methods for their use... Epidemiologic studies have clearly demonstrated that elevated blood pressure is correlated with an increased incidence of cardiovascular disease, including stroke, renal failure, congestive heart failure, and myocardial infarction. The prevalence of hypertension increases with age in all groups: blacks, whites, men, and women. Hypertension is an extremely common health problem in the geriatric population, afflicting approximately 65% of persons in the 65- to 74-year-old group (Bennett, J.C., and Plum, F., eds., Cecil's Textbook of Medicine, 20th ed., W. B. Saunders Co., Philadelphia, 1996, p. 258; this reference and others cited herein are expressly incorporated in their entireties by reference). Blacks have a higher prevalence of hypertension than whites, and men have a higher overall prevalence than women (ibid.). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Use of non-steroidal anti-inflammatory agents in combination with prostaglandin FP receptor agonists to treat glaucoma and ocular hypertension Inventor(s): Hellberg, Mark R. ; (Highland Village, TX), Nixon, Jon C. ; (Belhaven, NC) Correspondence: ALCON RESEARCH, LTD.; R&D COUNSEL, Q-148; 6201 SOUTH FREEWAY; FORT WORTH; TX; 76134-2099; US Patent Application Number: 20020103255 Date filed: January 28, 2002 Abstract: Disclosed are methods and compositions for the treatment of glaucoma and ocular hypertension, comprising the administration of a prostaglandin FP receptor agonist and a prostaglandin synthesis inhibitor. Excerpt(s): This application is a continuation-in-part of U.S. application Ser. No. 09/575,833 filed May 22, 2000, now U.S. Pat. No. 6,342,524, which is a continuation-inpart of U.S. application Ser. No. 08/994,903 filed Dec. 19, 1997, now U.S. Pat. No. 6,066,671... This invention is directed to the use of non-steroidal anti-inflammatory agents, and especially certain non-steroidal cyclooxygenase inhibitors in combination with prostaglandin FP receptor agonists for treating glaucoma and/or ocular hypertension in an individual... The glaucomas are a heterogeneous group of optic neuropathies characterized by cupping of the optic nerve head, thinning of the retinal nerve fiber layer due to loss of retinal ganglion cells, and specific pathognomonic changes in visual fields. Elevated intraocular pressure (IOP) is a very important risk factor for the development of most common forms of glaucoma (Sommer A, et al., "Relationship Between Intraocular Pressure and Primary Open Angle Glaucoma Among White and Black Americans," Arch. Ophthalmol, 109:1090-1095 (1991)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Vasopeptidase Inhibitors to treat isolated systolic hypertension Inventor(s): Wolf, Robert A. ; (Newton, PA), Reeves, Richard A. ; (Pennington, NJ), Chang, Paul I. ; (Doylestown, PA) Correspondence: MARLA J MATHIAS; BRISTOL-MYERS SQUIBB COMPANY; PATENT DEPARTMENT; P O BOX 4000; PRINCETON; NJ; 08543-4000; US Patent Application Number: 20020004500 Date filed: March 28, 2001 Abstract: Vasopeptidase inhibitors, especially omapatrilat, are useful in treating isolated systolic hypertension. The vasopeptidase inhibitor may be used in combination with other pharmaceutically active agents. Excerpt(s): Priority is claimed from U.S. provisional application 60/194,499 filed Apr. 3, 2000... Over the last several years compounds have been reported in the patent and technical literature as possessing in a single molecule both angiotensin converting enzyme (ACE) inhibitory activity and neutral endopeptidase (EC24.11; NEP) inhibition activity. These compounds are of interest as cardiovascular agents particularly in the treatment of hypertension, congestive heart failure, and renal disease. These compounds are also referred to as vasopeptidase, dual metalloprotease, NEP/ACE, or ACE/NEP
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inhibitors... Omapatrilat, its preparation, and its use in treating cardiovascular diseases are disclosed by Robl in U.S. Pat. No. 5,508,272. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Keeping Current In order to stay informed about patents and patent applications dealing with hypertension, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “hypertension” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on hypertension. You can also use this procedure to view pending patent applications concerning hypertension. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.
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CHAPTER 7. BOOKS ON HYPERTENSION Overview This chapter provides bibliographic book references relating to hypertension. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on hypertension include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “hypertension” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on hypertension: •
Atlas of Diseases of the Kidney. Volume 3: Hypertension and the Kidney Source: Philadelphia, PA: Current Medicine, Inc. 1999. [190 p.]. Contact: Available from Blackwell Science, Inc. 350 Main Street, Malden, MA 02148. (800) 215-1000 or (781) 388-8250. Fax (781) 388-8270. E-mail:
[email protected]. PRICE: $75.00 plus shipping and handling. ISBN: 063204389X. Summary: The kidney and hypertension are interrelated in cause and effect: renal parenchymal disease causes hypertension, and hypertension contributes to the progression of renal disease. This volume is the third in a series of five that make up the Atlas of Diseases of the Kidney, a set that offers educational images including colored photographs, schematics, tables, and algorithms. Volume 3, focuses on hypertension. It covers normal regulation of blood pressure and derangement in the common hypertension syndromes and finishes with a discussion of hypertension treatment. The volume begins with an overview of the regulation of normal blood pressure that
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describes the many integrated physiologic processes that regulate the body fluid volume and blood pressure. This is followed by a chapter on renal parenchymal hypertension and one on adrenal causes of hypertension. Although uncommon, these represent important diagnostic problems that require knowledge of the physiologic regulation of the adrenal gland in order to provide a rational approach to diagnosis and management. A separate chapter reviews diabetes, insulin resistance, and hypertension; another covers the role of hypertension in the progression of renal disease. The volume closes with two chapters devoted to treatment, including the major classes of antihypertensive agents available for treating hypertension, and an approach to hypertensive crisis. Each chapter features a detailed introduction and lengthy captions for each of the illustrations and diagrams offered. A subject index for Volume 3 and a section of full color plates concludes the book. •
Nephrology and Hypertension. 4th ed Source: Hagerstown, MD: Lippincott Williams and Wilkins. 1999. 368 p. Contact: Available from Lippincott Williams and Wilkins. P.O. Box 1600, Hagerstown, MD 21741. (800) 638-3030 or (301) 714-2300. Fax (301) 824-7390. Website: www.lww.com. PRICE: $26.95 plus shipping and handling. ISBN: 078172077X. Summary: Written by those who remember the information that was useful to them in their training, this book provides students, residents, and practitioners with basic clinical information on commonly encountered conditions in nephrology (kidney disease). Chapter 1 provides a brief overview of the structural and functional features of the kidney. Chapters 2 through 4 outline a practical approach to the functional and radiologic evaluation of the kidney, including the clinical indications for a kidney biopsy. Chapter 5 discusses the clinical significance of hematuria (blood in the urine) and identifies those clinical settings in which thorough evaluation is a necessity. In Chapter 6, the etiology, pathophysiology, and method of evaluation of proteinuria (protein in the urine) and the nephrotic syndrome are presented. Chapter 7 reviews diabetic nephropathy; then Chapter 8 discusses several forms of renal disease that are glomerular in type, including minimal change disease, focal segmental glomerulosclerosis, membranous glomerulonephritis, post infectious proliferative glomerulonephritis, and IgA nephropathy. Chapter 9 describes the various types of glomerulonephritis observed in patients with systemic lupus erythematosus (SLE). In Chapter 10, the problem of vasculitis is addressed in its many forms, including Wegener's granulomatosis, polyarteritis nodosa, and Schonlein Henoch purpura. Chapter 11 provides descriptions of the renal (kidney) manifestations of the thrombotic microangiopathies, progressive systemic sclerosis, multiple myeloma, and amyloidosis. Chapter 12 discusses tubulointerstitial nephritis, and Chapter 13 reviews the more frequently encountered familial and cystic forms of renal disease. Chapter 14 covers HIV infection and the kidney, including management of HIV infected patients with acute or chronic renal failure. The next section contains four chapters on disorders of water, electrolytes, and acid base regulation. In Chapter 19 renal stone disease is reviewed; Chapter 20 covers urinary tract infection (UTI). The next five chapters cover the diagnosis and management of hypertension (high blood pressure) and the use of diuretics in clinical practice. The last section covers diagnosis and management of renal failure; six chapters cover dialysis, patient care management, the role of nutrition in managing kidney failure, and drug therapy for acute and chronic renal failure. Each chapter concludes with a list of suggested readings, and the handbook concludes with a subject index.
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Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “hypertension” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “hypertension” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “hypertension” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
100 Questions and Answers About Hypertension by William M., Md Manger, Ray W., Jr Gifford; ISBN: 0632044810; http://www.amazon.com/exec/obidos/ASIN/0632044810/icongroupinterna
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6th International Adalat Symposium: New Therapy of Ischaemic Heart Disease and Hypertension (Current Clinical Practice Series, 41) by P.R. Lichtlen (Editor) (1986); ISBN: 0444904492; http://www.amazon.com/exec/obidos/ASIN/0444904492/icongroupinterna
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A Beginner's Guide to Shiatsu: Using Japanese Finger Pressure for the Relief of Headaches, Back Pain, and Hypertension by Patrick McCarty (1995); ISBN: 0895296594; http://www.amazon.com/exec/obidos/ASIN/0895296594/icongroupinterna
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A Century of Arterial Hypertension : 1896 - 1996 by Nicolas Postel-Vinay (Editor) (1997); ISBN: 0471967882; http://www.amazon.com/exec/obidos/ASIN/0471967882/icongroupinterna
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A Color Atlas of Hypertension (1991); ISBN: 0723416370; http://www.amazon.com/exec/obidos/ASIN/0723416370/icongroupinterna
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A Color Atlas of Hypertension by Leonard M. Shapiro, Maurice B. Buchalter; ISBN: 0815176635; http://www.amazon.com/exec/obidos/ASIN/0815176635/icongroupinterna
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A Physician's Guide to Hypertension by William B. White; ISBN: 0824782313; http://www.amazon.com/exec/obidos/ASIN/0824782313/icongroupinterna
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A Slide Atlas of Hypertension by G. B. M. Lindop, Peter F. Semple; ISBN: 1850705526; http://www.amazon.com/exec/obidos/ASIN/1850705526/icongroupinterna
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ABC of Hypertension by E. O'Brien, D.G. Beevers (1987); ISBN: 0727901931; http://www.amazon.com/exec/obidos/ASIN/0727901931/icongroupinterna
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ABC's of Antihypertensive Therapy by Franz Messerli (1994); ISBN: 1881063038; http://www.amazon.com/exec/obidos/ASIN/1881063038/icongroupinterna
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Ace Inhibitors in Hypertension: A Guide for General Practitioners by Gillian Strube, George Strubve (1992); ISBN: 0792389638; http://www.amazon.com/exec/obidos/ASIN/0792389638/icongroupinterna
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Adrenal Glands, Vascular System and Hypertension by D. C. Anderson, Gavin P. Vinson (1996); ISBN: 1898099073; http://www.amazon.com/exec/obidos/ASIN/1898099073/icongroupinterna
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Advances in Hypertension by Kotchen (1993); ISBN: 0397513321; http://www.amazon.com/exec/obidos/ASIN/0397513321/icongroupinterna
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Aerobic Walking The Weight-Loss Exercise : A Complete Program to Reduce Weight, Stress, and Hypertension by Mort Malkin (Author) (1995); ISBN: 0471556726; http://www.amazon.com/exec/obidos/ASIN/0471556726/icongroupinterna
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All You Wanted to Know About Hypertension by Savitri Ramaiah (Editor); ISBN: 8120722280; http://www.amazon.com/exec/obidos/ASIN/8120722280/icongroupinterna
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An Atlas of Hypertension, Second Edition by Peter F. Semple, George B. M. Lindop; ISBN: 1850709491; http://www.amazon.com/exec/obidos/ASIN/1850709491/icongroupinterna
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An Illustrated Pocketbook of Hypertension by Peter F. Semple; ISBN: 1842140574; http://www.amazon.com/exec/obidos/ASIN/1842140574/icongroupinterna
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Antihypertensive agents; ISBN: 3540075941; http://www.amazon.com/exec/obidos/ASIN/3540075941/icongroupinterna
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Antihypertensive agents : a symposium sponsored by the Division of Medicinal Chemistry at the 169th meeting of the American Chemical Society, Philadelphia, Penn., April 8, 1975; ISBN: 0841203334; http://www.amazon.com/exec/obidos/ASIN/0841203334/icongroupinterna
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Arterial and Venous Systems in Essential Hypertension (Developments in Cardiovascular Medicine) by Michel Safar (Editor), et al (1988); ISBN: 0898388570; http://www.amazon.com/exec/obidos/ASIN/0898388570/icongroupinterna
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Arterial Baroreceptors and Hypertension by Peter Sleight (Editor); ISBN: 019261259X; http://www.amazon.com/exec/obidos/ASIN/019261259X/icongroupinterna
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Arterial Hypertension (Bailliere's Clinical Anaesthesiology); ISBN: 0702023604; http://www.amazon.com/exec/obidos/ASIN/0702023604/icongroupinterna
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Arterial hypertension : proceedings of the first international sympoium, Caracas, Venezuela, 1-3 September 1976; ISBN: 0444152601; http://www.amazon.com/exec/obidos/ASIN/0444152601/icongroupinterna
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Arterial Hypertension, Pathogenesis, Diagnosis and Therapy: Monograph by Julian Rosenthal (Editor); ISBN: 0387906118; http://www.amazon.com/exec/obidos/ASIN/0387906118/icongroupinterna
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Arteries in Clinical Hypertension by Michel Safar; ISBN: 0397514840; http://www.amazon.com/exec/obidos/ASIN/0397514840/icongroupinterna
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Aspects of Hypertension Management by Gordon Mallarkey (Editor) (2000); ISBN: 0864710577; http://www.amazon.com/exec/obidos/ASIN/0864710577/icongroupinterna
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Atherosclerosis, Hypertension and Diabetes (Progress in Experimental Cardiology, 8) by Grant N., Ph.D. Pierce (Editor), et al; ISBN: 1402073119; http://www.amazon.com/exec/obidos/ASIN/1402073119/icongroupinterna
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Atlas of Hypertension by Norman K. Hollenberg (Editor) (2003); ISBN: 157340196X; http://www.amazon.com/exec/obidos/ASIN/157340196X/icongroupinterna
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Behavioral Factors in Hypertension (Handbook of Hypertension, Vol 9) by Stevo Julius, et al; ISBN: 0444904778; http://www.amazon.com/exec/obidos/ASIN/0444904778/icongroupinterna
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Beta-Blockers in Hypertension and Angina Pectoris: Different Compounds, Different Strategies by Ton J. M. Cleophas (1995); ISBN: 0792335163; http://www.amazon.com/exec/obidos/ASIN/0792335163/icongroupinterna
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Biologically Active Atrial Peptides (American Society of Hypertension Series Vol 1) by Barry M. Brenner, John H. Laragh (Editor); ISBN: 0881673064; http://www.amazon.com/exec/obidos/ASIN/0881673064/icongroupinterna
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Blood Cells and Arteries in Hypertension and Atherosclerosis (Atherosclerosis Reviews, Vol 19) by Philippe Meyer, Pierre Marche (Editor) (1989); ISBN: 0881674753; http://www.amazon.com/exec/obidos/ASIN/0881674753/icongroupinterna
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Blood Vessel Changes in Hypertension Structure and Function, Volume I by Robert M.K.W. Lee (Editor), et al; ISBN: 0849348838; http://www.amazon.com/exec/obidos/ASIN/0849348838/icongroupinterna
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Breathe Well, Be Well : A Program to Relieve Stress, Anxiety, Asthma, Hypertension, Migraine, and Other Disorders for Better Health by Robert Fried (Author); ISBN: 0471324361; http://www.amazon.com/exec/obidos/ASIN/0471324361/icongroupinterna
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Calcium & Hypertension by Shaul G. Massry (Editor), Carlo Gennari (Editor) (1987); ISBN: 3805543700; http://www.amazon.com/exec/obidos/ASIN/3805543700/icongroupinterna
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Calcium Antagonists and Hypertension: Current Status (Current Clinical Practice Series, 39) by J. Rosenthal (Editor); ISBN: 0444904557; http://www.amazon.com/exec/obidos/ASIN/0444904557/icongroupinterna
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Calcium Antagonists in the Treatment of Hypertension in Pregnancy by A. L. Tranquilli (Editor), C. Romanini; ISBN: 1850704686; http://www.amazon.com/exec/obidos/ASIN/1850704686/icongroupinterna
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Calcium in Essential Hypertension by Kyuzo Aoki, Edward D. Frohlich (Editor); ISBN: 0120588455; http://www.amazon.com/exec/obidos/ASIN/0120588455/icongroupinterna
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Cardiovascular Risk Factors in Children: The Early Natural History of Atherosclerosis and Essential Hypertension by Gerald S. Berenson; ISBN: 019502589X; http://www.amazon.com/exec/obidos/ASIN/019502589X/icongroupinterna
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Cellular and Molecular Mechanisms in Hypertension (Advances in Experimental Medicine and Biology, 308) by Robert H. Cox (Editor) (1992); ISBN: 0306440849; http://www.amazon.com/exec/obidos/ASIN/0306440849/icongroupinterna
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Cellular Aspects of Hypertension by G. Bruschi, A. Borghetti (Editor); ISBN: 0387539875; http://www.amazon.com/exec/obidos/ASIN/0387539875/icongroupinterna
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Cellular aspects of hypertension; ISBN: 3540539875; http://www.amazon.com/exec/obidos/ASIN/3540539875/icongroupinterna
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Central and Peripheral Sympathetic Mechanisms in Hypertension: Pathophysiological and Therapeutic Aspects. Focus on Urapidil: Pathophysiological and Therapeutic Aspects. Focus on Urapidil : Proceedings. Edited by P.A. Van Zwieten (International Congress and Symposium Series (ICSS)) by P.A. Van Zwieten (Editor); ISBN: 1853151939; http://www.amazon.com/exec/obidos/ASIN/1853151939/icongroupinterna
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Central Nervous System Mechanisms in Hypertension by Joseph P. Buckley (Editor), Carlos Ferrario (Editor); ISBN: 0890045453; http://www.amazon.com/exec/obidos/ASIN/0890045453/icongroupinterna
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Chesley's Hypertensive Disorders in Pregnancy by Marshall D., MD Lindheimer (Editor), et al; ISBN: 083853970X; http://www.amazon.com/exec/obidos/ASIN/083853970X/icongroupinterna
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Chronic Disease Management on Disk: Hypertension by Aspen Reference Group, Aspen (1998); ISBN: 0834209985; http://www.amazon.com/exec/obidos/ASIN/0834209985/icongroupinterna
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Clinical Aspects of Renovascular Hypertension by R. Van Schilfgaarde (1983); ISBN: 0898385741; http://www.amazon.com/exec/obidos/ASIN/0898385741/icongroupinterna
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Clinical Aspects of Secondary Hypertension (Handbook of Hypertension, Vol. 2) by J. I. S. Robertson (Editor); ISBN: 0444903089; http://www.amazon.com/exec/obidos/ASIN/0444903089/icongroupinterna
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Clinical Atlas of Hypertension by John D. Swales, et al; ISBN: 0397445822; http://www.amazon.com/exec/obidos/ASIN/0397445822/icongroupinterna
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Clinical Guide to Hypertension by Timothy N. Caris; ISBN: 0884164772; http://www.amazon.com/exec/obidos/ASIN/0884164772/icongroupinterna
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Clinical Hypertension by J. I. S. Robertson (Editor); ISBN: 0444812946; http://www.amazon.com/exec/obidos/ASIN/0444812946/icongroupinterna
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Clinical hypertension by Norman M. Kaplan; ISBN: 0683045148; http://www.amazon.com/exec/obidos/ASIN/0683045148/icongroupinterna
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Clinical Hypertension in Nephrology: International Meeting, Lido Degli Aranci, Calabria, September 20-23, 1995 (Contributions to Nephrology, Vol. 119) by Carmine Zoccali (Editor) (1996); ISBN: 3805563019; http://www.amazon.com/exec/obidos/ASIN/3805563019/icongroupinterna
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Clinical Hypertension in Practice by Gregory Y. H. Lip (2003); ISBN: 1853154857; http://www.amazon.com/exec/obidos/ASIN/1853154857/icongroupinterna
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Clinical Management of Hypertension in Diabetes by Anthony H. Barnett (2003); ISBN: 1841840793; http://www.amazon.com/exec/obidos/ASIN/1841840793/icongroupinterna
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Clinical Management of Hypertension, Sixth Edition by Marvin Moser; ISBN: 1884735738; http://www.amazon.com/exec/obidos/ASIN/1884735738/icongroupinterna
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Clinical Pulmonary Hypertension (Portland Press Research Monograph, 8) by A. K. Morice (Editor) (1995); ISBN: 1855780747; http://www.amazon.com/exec/obidos/ASIN/1855780747/icongroupinterna
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Clinical Research in Essential Hypertension by Michel Safar; ISBN: 3794512782; http://www.amazon.com/exec/obidos/ASIN/3794512782/icongroupinterna
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Clinical Trials in Hypertension by Henry R. Black (Editor) (2001); ISBN: 0824702700; http://www.amazon.com/exec/obidos/ASIN/0824702700/icongroupinterna
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Clinician's Manual on Combination Therapy in Hypertension by Messerli (2002); ISBN: 1858739500; http://www.amazon.com/exec/obidos/ASIN/1858739500/icongroupinterna
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Clinician's Manual on Hypertension, Diabetes Mellitus, and Nephropathy by J. G. Porush, F. Faubert (2001); ISBN: 1858739012; http://www.amazon.com/exec/obidos/ASIN/1858739012/icongroupinterna
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Clinician's Manual on Target Organ Damage in Hypertension by A.H. Barnett (Editor), P.M. Dodson (Editor) (1997); ISBN: 1858730465; http://www.amazon.com/exec/obidos/ASIN/1858730465/icongroupinterna
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Combination Drug Therapy in Hypertension - pocketbook by Michael Schachter, Michael Schacter; ISBN: 1853177326; http://www.amazon.com/exec/obidos/ASIN/1853177326/icongroupinterna
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Comparative Studies in Hypertension by H. Vetter, et al (1987); ISBN: 3805547102; http://www.amazon.com/exec/obidos/ASIN/3805547102/icongroupinterna
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Conquering High Blood Pressure: The Complete Guide to Managing Hypertension by Stephen Wood, et al; ISBN: 0306456311; http://www.amazon.com/exec/obidos/ASIN/0306456311/icongroupinterna
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Conquering Hypertension: An Illustrated Guide to Understanding Treatment and Control of High Blood Pressure by R. Brian Haynes MD, Frans H. H. Leenen (1994); ISBN: 0969778120; http://www.amazon.com/exec/obidos/ASIN/0969778120/icongroupinterna
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Contemporary Diagnosis and Management of Hypertension in African Americans by Elijah Saunders, Wallace R. Johnson; ISBN: 1884065716; http://www.amazon.com/exec/obidos/ASIN/1884065716/icongroupinterna
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Contemporary Diagnosis and Management of Hypertension® by Myron H. Weinberger; ISBN: 1884065147; http://www.amazon.com/exec/obidos/ASIN/1884065147/icongroupinterna
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Control High Blood Pressure Without Drugs: A Complete Hypertension Handbook by Robert L., Md Rowan, Constance Schrader (Contributor) (2001); ISBN: 0684873281; http://www.amazon.com/exec/obidos/ASIN/0684873281/icongroupinterna
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Control mechanisms in essential hypertension by W. H. Birkenhäger; ISBN: 0444414525; http://www.amazon.com/exec/obidos/ASIN/0444414525/icongroupinterna
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Controversies in Nephrology and Hypertension by Robert G. Narins (Editor) (1984); ISBN: 0443082383; http://www.amazon.com/exec/obidos/ASIN/0443082383/icongroupinterna
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Crisis Obstetrics: Hypertension in Pregnancy (Part 3) by Judy Poole (1995); ISBN: 0815168322; http://www.amazon.com/exec/obidos/ASIN/0815168322/icongroupinterna
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Current Concept in the Therapy of Hypertension with Beta-Blockers by S. Chaithiraphan (1980); ISBN: 380550912X; http://www.amazon.com/exec/obidos/ASIN/380550912X/icongroupinterna
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Current Management of Hypertensive and Vascular Diseases (Current Therapy Series) by John P. Cooke, Edward D. Frohlich; ISBN: 155664356X; http://www.amazon.com/exec/obidos/ASIN/155664356X/icongroupinterna
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Current Therapy in Nephrology and Hypertension by Richard J. Glassock (Editor) (1998); ISBN: 0815137338; http://www.amazon.com/exec/obidos/ASIN/0815137338/icongroupinterna
340 Hypertension
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Current Therapy in Nephrology and Hypertension, 1984-1985 by Richard J. Glassock (1984); ISBN: 0941158306; http://www.amazon.com/exec/obidos/ASIN/0941158306/icongroupinterna
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Diabetes Mellitus and Hypertension (Managing Major Diseases) by Laura Ninger, et al (1999); ISBN: 0815120400; http://www.amazon.com/exec/obidos/ASIN/0815120400/icongroupinterna
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Diagnosis and Management of Renal Disease and Hypertension by Anil K. Mandal (Editor), J. Charles Jennette (Editor) (1994); ISBN: 0890895570; http://www.amazon.com/exec/obidos/ASIN/0890895570/icongroupinterna
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Diagnosis and Management of Renal Disease and Hypertension (1994); ISBN: 081211129X; http://www.amazon.com/exec/obidos/ASIN/081211129X/icongroupinterna
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Diagnostic Picture Tests in Hypertension by Graham A. MacGregor; ISBN: 0723424772; http://www.amazon.com/exec/obidos/ASIN/0723424772/icongroupinterna
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Diagnostic Reasoning Series - Hypertension (CD-ROM) by Accredited by the AMA; ISBN: 0914168495; http://www.amazon.com/exec/obidos/ASIN/0914168495/icongroupinterna
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Die portale Hypertension : Pathophysiologie, Diagnostik, Therapie; ISBN: 3879210454; http://www.amazon.com/exec/obidos/ASIN/3879210454/icongroupinterna
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Diseases Explained: Hypertension Wall Chart by Lexi-Comp; ISBN: 1930598114; http://www.amazon.com/exec/obidos/ASIN/1930598114/icongroupinterna
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Diuresis, kaliuresis, and hypertension : long-term clinical experience with a fixed combination of amiloride hydrochloride and hydrochlorothiazide; ISBN: 0879931078; http://www.amazon.com/exec/obidos/ASIN/0879931078/icongroupinterna
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Diuretics in Hypertension and in Heart Failure (Progress in Pharmacology and Clinical Pharmacology, Vol 10, No 3) by Ariel J. Reyes (Editor) (1995); ISBN: 3437116142; http://www.amazon.com/exec/obidos/ASIN/3437116142/icongroupinterna
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Drug Therapy in Hypertension by Jan I.M. Drayer, et al; ISBN: 0824775058; http://www.amazon.com/exec/obidos/ASIN/0824775058/icongroupinterna
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Eat to Beat - High Blood Pressure: Natural Self-help for Hypertension, Including 60 Recipes (Eat to Beat) by Sarah Brewer, Michelle Berridale-Johnson; ISBN: 0007141351; http://www.amazon.com/exec/obidos/ASIN/0007141351/icongroupinterna
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Eating Well, Living Well With Hypertension (Eating Well Living Well) by Laura P. Svetkey, et al; ISBN: 067086658X; http://www.amazon.com/exec/obidos/ASIN/067086658X/icongroupinterna
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Endocrine Hypertension (Annals of the New York Academy of Sciences, Vol 970) by International Workshop on Endocrine Hypertension 2001, et al (2002); ISBN: 1573314188; http://www.amazon.com/exec/obidos/ASIN/1573314188/icongroupinterna
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Endocrine Hypertension (Comprehensive Endocrinology, Revised Series) by Edward G., M.D. Biglieri, James C., M.D. Melby (Editor) (1990); ISBN: 0881675873; http://www.amazon.com/exec/obidos/ASIN/0881675873/icongroupinterna
Books 341
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Endocrine Mechanisms in Hypertension (Perspectives in Hypertension Series, Vol 2) by John H. Laragh, et al (1989); ISBN: 0881674796; http://www.amazon.com/exec/obidos/ASIN/0881674796/icongroupinterna
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Endocrinology of Hypertension: Proceedings of the Serono Symposia by F. Biglieri, E.G. and Edwards, C.R.W. Mantero (Editor), et al; ISBN: 0124699804; http://www.amazon.com/exec/obidos/ASIN/0124699804/icongroupinterna
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Endothelial Function in Hypertension by D. Webb (Editor), P. Vallance (Editor) (1997); ISBN: 3540629432; http://www.amazon.com/exec/obidos/ASIN/3540629432/icongroupinterna
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Epidemiology and control of hypertension : papers and discussions from the second International Symposium on the Epidemiology of Hypertension presented September 1974 by the Chicago Heart Association. [et al.]; ISBN: 0883720264; http://www.amazon.com/exec/obidos/ASIN/0883720264/icongroupinterna
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Epidemiology of Hypertension by C. J. Bulpitt (Editor); ISBN: 044482779X; http://www.amazon.com/exec/obidos/ASIN/044482779X/icongroupinterna
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Ergometry in Hypertensive Patients: Implications for Diagnosis and Treatment by Ingomar-Werner Franz (1986); ISBN: 0387153225; http://www.amazon.com/exec/obidos/ASIN/0387153225/icongroupinterna
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Essential Guide to Hypertension by American Medical Association (Editor) (2000); ISBN: 0743403606; http://www.amazon.com/exec/obidos/ASIN/0743403606/icongroupinterna
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Essential Hypertension by Timothy N. Caris; ISBN: 0945892012; http://www.amazon.com/exec/obidos/ASIN/0945892012/icongroupinterna
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Essential Hypertension 2 by Kyuzo Aoki (Editor); ISBN: 0387700447; http://www.amazon.com/exec/obidos/ASIN/0387700447/icongroupinterna
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Essential Hypertension As an Endocrine Disease (Butterworth's International Medical Reviews/Clinical Endocrinology, Vol 3) by Christopher R.W. Edwards, Robert M. Carey (Editor) (1985); ISBN: 0407022740; http://www.amazon.com/exec/obidos/ASIN/0407022740/icongroupinterna
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Essential Hypertension: Calcium Mechanisms and Treatment by K. Aoki (Editor) (1987); ISBN: 0387700161; http://www.amazon.com/exec/obidos/ASIN/0387700161/icongroupinterna
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Evidence-based Hypertension by Cynthia D. Mulrow (Editor); ISBN: 0727914383; http://www.amazon.com/exec/obidos/ASIN/0727914383/icongroupinterna
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Experimental and Genetic Models of Hypertension by D. Ganten (Editor), et al; ISBN: 0444897151; http://www.amazon.com/exec/obidos/ASIN/0444897151/icongroupinterna
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Experimental Hypertension and Therapeutic Progress: Vasodilation and Beyond by B. Garthoff (1995); ISBN: 0387585451; http://www.amazon.com/exec/obidos/ASIN/0387585451/icongroupinterna
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Fact Book on Hypertension High Blood Pressure and Your Diet by Carlson Wade; ISBN: 0879830956; http://www.amazon.com/exec/obidos/ASIN/0879830956/icongroupinterna
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Fifth International Adalat Symposium: New Therapy of Ischaemic Heart Disease and Hypertension (Current Clinical Practice Series, No. 2) by International Adalat
342 Hypertension
Registered Trademark Symbol Symposium 1982 Berli, et al (1983); ISBN: 0444903119; http://www.amazon.com/exec/obidos/ASIN/0444903119/icongroupinterna •
From Hypertension to Heart Failure by J.G.F. Cleland, J. McMurray (1995); ISBN: 1858730597; http://www.amazon.com/exec/obidos/ASIN/1858730597/icongroupinterna
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Fundamental Fault in Hypertension (Developments in Cardiovascular Medicine, 36) by Mohinder P. Sambhi (Editor) (1984); ISBN: 0898386381; http://www.amazon.com/exec/obidos/ASIN/0898386381/icongroupinterna
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Genetic Approaches of Coronary Heart Disease and Hypertension by Kare Berg (1991); ISBN: 3540544763; http://www.amazon.com/exec/obidos/ASIN/3540544763/icongroupinterna
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Genetic Hypertension by J. Sassard (Editor) (1996); ISBN: 2855984858; http://www.amazon.com/exec/obidos/ASIN/2855984858/icongroupinterna
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Genetic hypertension : proceedings of the 7th International Symposium on SHR and Related Studies held in Lyon (France), Ecole Normale Supérieure, October 28-30, 1991 = Hypertension génétique; ISBN: 086196313X; http://www.amazon.com/exec/obidos/ASIN/086196313X/icongroupinterna
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Genetic Immune and Molecular Predisposition to Hypertension (Progress in Hypertension) by P. M. Frossard (Editor), et al (1999); ISBN: 9067643114; http://www.amazon.com/exec/obidos/ASIN/9067643114/icongroupinterna
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Good News About High Blood Pressure: Everything You Need to Know to Take Control of Hypertension--And Your Life by Thomas Pickering (1996); ISBN: 0684813963; http://www.amazon.com/exec/obidos/ASIN/0684813963/icongroupinterna
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Handbook of Antihypertensive Therapy by Mark D., Md, Facp Houston, et al (2000); ISBN: 1560534222; http://www.amazon.com/exec/obidos/ASIN/1560534222/icongroupinterna
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Healing Hypertension: A Revolutionary New Approach by Samuel J. Mann (Author); ISBN: 0471376434; http://www.amazon.com/exec/obidos/ASIN/0471376434/icongroupinterna
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Heart Attacks, Hypertension, and Heart Drugs by M. Gabriel Khan; ISBN: 0878577106; http://www.amazon.com/exec/obidos/ASIN/0878577106/icongroupinterna
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Heart Disease, Hypertension and Nutrition by Health Media of America, Alisonn Nhull (1986); ISBN: 0937325066; http://www.amazon.com/exec/obidos/ASIN/0937325066/icongroupinterna
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Heterogeneity of Renin and Renin-Substrate: Proceedings of the Seventh Scientific Meeting of the International Society of Hypertension, New Orleans, by Sambhi; ISBN: 0444006184; http://www.amazon.com/exec/obidos/ASIN/0444006184/icongroupinterna
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High Blood Pressure: Practical, Medical, and Spiritual Guidelines for Daily Living With Hypertension (Hazelden Pocket Health Guide) by Mark Jenkins; ISBN: 1568383517; http://www.amazon.com/exec/obidos/ASIN/1568383517/icongroupinterna
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High Blood Pressure: The Black Man and Woman's Guide to Living with Hypertension by Hilton M., Ii Hudson, et al (2002); ISBN: 0971606714; http://www.amazon.com/exec/obidos/ASIN/0971606714/icongroupinterna
Books 343
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How Free Care Reduced Hypertension of Participants in the Rand Health Insurance Experiment by Emmett B. Keeler (1985); ISBN: 0833006827; http://www.amazon.com/exec/obidos/ASIN/0833006827/icongroupinterna
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How I lost fifty pounds and got off hypertension medication by Charlie F. Loftin; ISBN: 0964757907; http://www.amazon.com/exec/obidos/ASIN/0964757907/icongroupinterna
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How Should Elderly Hypertensive Patients Be Treated? (1989); ISBN: 3540700404; http://www.amazon.com/exec/obidos/ASIN/3540700404/icongroupinterna
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How Should Elderly Hypertensive Patients Be Treated?: Proceedings of Satellite Symposium to the 12th Scientific Meeting of the International Society by A. Zanchetti (Editor), Teruo Omae (1989); ISBN: 0387700404; http://www.amazon.com/exec/obidos/ASIN/0387700404/icongroupinterna
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How to Lower High Blood Pressure: The Natural Way to Reduce Hypertension by Caroline M. Shreeve (2001); ISBN: 000712094X; http://www.amazon.com/exec/obidos/ASIN/000712094X/icongroupinterna
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Hypertension by John H. Laragh; ISBN: 091431601X; http://www.amazon.com/exec/obidos/ASIN/091431601X/icongroupinterna
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Hypertension by Stephen Bell; ISBN: 0944132596; http://www.amazon.com/exec/obidos/ASIN/0944132596/icongroupinterna
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Hypertension by Lennart Hansen (Editor), et al; ISBN: 0077095235; http://www.amazon.com/exec/obidos/ASIN/0077095235/icongroupinterna
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Hypertension by Norman M Kaplan; ISBN: 0397505507; http://www.amazon.com/exec/obidos/ASIN/0397505507/icongroupinterna
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Hypertension; ISBN: 040702266X; http://www.amazon.com/exec/obidos/ASIN/040702266X/icongroupinterna
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Hypertension by G. Pickering; ISBN: 0443011249; http://www.amazon.com/exec/obidos/ASIN/0443011249/icongroupinterna
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Hypertension (1988); ISBN: 0443016658; http://www.amazon.com/exec/obidos/ASIN/0443016658/icongroupinterna
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Hypertension by Villarreal; ISBN: 0471079006; http://www.amazon.com/exec/obidos/ASIN/0471079006/icongroupinterna
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Hypertension by Peter A. Meredith, et al (2003); ISBN: 0723433151; http://www.amazon.com/exec/obidos/ASIN/0723433151/icongroupinterna
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Hypertension by Brady; ISBN: 0876180802; http://www.amazon.com/exec/obidos/ASIN/0876180802/icongroupinterna
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Hypertension (1995); ISBN: 0881674931; http://www.amazon.com/exec/obidos/ASIN/0881674931/icongroupinterna
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Hypertension by Eugene Braunwald (1997); ISBN: 1573400564; http://www.amazon.com/exec/obidos/ASIN/1573400564/icongroupinterna
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Hypertension by Lisa Henderson; ISBN: 1930624042; http://www.amazon.com/exec/obidos/ASIN/1930624042/icongroupinterna
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Hypertension - Evaluation and Treatment [DOWNLOAD: PDF] by Apollo Managed Care Consultants (Author); ISBN: B000064765; http://www.amazon.com/exec/obidos/ASIN/B000064765/icongroupinterna
344 Hypertension
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Hypertension - Hot Topics by Brent M., Md Egan, et al; ISBN: 1560535784; http://www.amazon.com/exec/obidos/ASIN/1560535784/icongroupinterna
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Hypertension (Clinical Series) by John Coope (1993); ISBN: 0850841860; http://www.amazon.com/exec/obidos/ASIN/0850841860/icongroupinterna
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Hypertension (Contemporary Issues in Nephrology Series, Vol 8) by Barry M. Brenner, Jay H. Stein (Editor) (1981); ISBN: 044308145X; http://www.amazon.com/exec/obidos/ASIN/044308145X/icongroupinterna
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Hypertension (Hypertension Series) by Robert L. Bloomfield (Editor), et al; ISBN: 0890895457; http://www.amazon.com/exec/obidos/ASIN/0890895457/icongroupinterna
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Hypertension (Pathophysiology for Nurses Series) by Blanchard, et al (2000); ISBN: 1930138024; http://www.amazon.com/exec/obidos/ASIN/1930138024/icongroupinterna
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Hypertension (Pocket Doc Library Patient Guide) by Randy J. Shields, William Frishman (1997); ISBN: 1888886005; http://www.amazon.com/exec/obidos/ASIN/1888886005/icongroupinterna
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Hypertension (Practical Clinical Medicine Series) by Gerald Sandler (1988); ISBN: 0746200412; http://www.amazon.com/exec/obidos/ASIN/0746200412/icongroupinterna
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Hypertension : a practitioner's guide to therapy by James C. Hutchison; ISBN: 0874887097; http://www.amazon.com/exec/obidos/ASIN/0874887097/icongroupinterna
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Hypertension : The Guide to Keeping Blood Pressure Down by Ifeoma, MD Ezekwo (2001); ISBN: 1930927002; http://www.amazon.com/exec/obidos/ASIN/1930927002/icongroupinterna
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Hypertension : The Silent Killer by Hasnain, Ph.D. Walji, Hasnain Walji; ISBN: 1891294067; http://www.amazon.com/exec/obidos/ASIN/1891294067/icongroupinterna
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Hypertension 2003 Weekly Planner: High Blood Pressure by Bonnie Dickens, Thomas Masterson; ISBN: 1588082083; http://www.amazon.com/exec/obidos/ASIN/1588082083/icongroupinterna
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Hypertension After Menopause by M. Stimpel (Editor), A. Zanchetti (Editor) (1996); ISBN: 3110155184; http://www.amazon.com/exec/obidos/ASIN/3110155184/icongroupinterna
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Hypertension and Co-Existing Disease by Francisco Leyva, et al; ISBN: 063205073X; http://www.amazon.com/exec/obidos/ASIN/063205073X/icongroupinterna
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Hypertension and cognitive processes; ISBN: 0933786042; http://www.amazon.com/exec/obidos/ASIN/0933786042/icongroupinterna
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Hypertension and Diabetes by Barnett, Dodson (2000); ISBN: 1858739020; http://www.amazon.com/exec/obidos/ASIN/1858739020/icongroupinterna
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Hypertension and Nutrition by Eric R. Braverman, et al; ISBN: 0879836881; http://www.amazon.com/exec/obidos/ASIN/0879836881/icongroupinterna
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Hypertension and Renal Disease (Contributions to Nephrology, Vol 54) by V.M. Campese, et al (1987); ISBN: 3805543727; http://www.amazon.com/exec/obidos/ASIN/3805543727/icongroupinterna
Books 345
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Hypertension and Renal Disease in the Elderly by Manuel Maldonado-Martinez (Editor); ISBN: 0865420939; http://www.amazon.com/exec/obidos/ASIN/0865420939/icongroupinterna
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Hypertension and Stress: A Unified Concept by Alvin P., MD Shapiro (1996); ISBN: 0805819045; http://www.amazon.com/exec/obidos/ASIN/0805819045/icongroupinterna
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Hypertension and the Angiotensin System: Therapeutic Approaches by Alexander G. Bearn (Editor), Austin Eric Doyle (Editor) (1984); ISBN: 0890043094; http://www.amazon.com/exec/obidos/ASIN/0890043094/icongroupinterna
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Hypertension and the Brain by Gordon P. Guthrie (1984); ISBN: 0879932112; http://www.amazon.com/exec/obidos/ASIN/0879932112/icongroupinterna
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Hypertension and the Heart by Alberto Zanchetti (Editor), et al; ISBN: 0306457741; http://www.amazon.com/exec/obidos/ASIN/0306457741/icongroupinterna
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Hypertension Arterielle Des Populations Originaires D' Afrique Bertrand; ISBN: 2907516582; http://www.amazon.com/exec/obidos/ASIN/2907516582/icongroupinterna
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Hypertension Calendar and Weekly Planner 2002 by International Medical Publishing, et al; ISBN: 1588080684; http://www.amazon.com/exec/obidos/ASIN/1588080684/icongroupinterna
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Hypertension Care: A Guide for Patient Education by Shirley Muson, Shirley Coggins Mason; ISBN: 0838539939; http://www.amazon.com/exec/obidos/ASIN/0838539939/icongroupinterna
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Hypertension Control for Nurses and Other Health Professionals (1985); ISBN: 0801627176; http://www.amazon.com/exec/obidos/ASIN/0801627176/icongroupinterna
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Hypertension Control for Nurses and Other Health Professionals by Mahendr S. Kocher, Karyn D. Woods (1985); ISBN: 0826146414; http://www.amazon.com/exec/obidos/ASIN/0826146414/icongroupinterna
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HYPERTENSION DIAGNOSTICS, INC.: International Competitive Benchmarks and Financial Gap Analysis (Financial Performance Series) by Icon Group Ltd., Icon Group Ltd. ISBN: 0597380414; http://www.amazon.com/exec/obidos/ASIN/0597380414/icongroupinterna
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HYPERTENSION DIAGNOSTICS, INC.: Labor Productivity Benchmarks and International Gap Analysis (Labor Productivity Series) by Icon Group Ltd., Icon Group Ltd. ISBN: 0597449805; http://www.amazon.com/exec/obidos/ASIN/0597449805/icongroupinterna
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Hypertension Digest : Learn Why High Blood Pressure Is Such a Danger [DOWNLOAD: PDF]; ISBN: B00009KF23; http://www.amazon.com/exec/obidos/ASIN/B00009KF23/icongroupinterna
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Hypertension Essentials by Norman M. Kaplan, Micheal A. Weber (2003); ISBN: 1890114448; http://www.amazon.com/exec/obidos/ASIN/1890114448/icongroupinterna
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Hypertension Essentials: Current Concepts of Cause and Control by Theodore Goodfriend (Editor); ISBN: 0808915835; http://www.amazon.com/exec/obidos/ASIN/0808915835/icongroupinterna
346 Hypertension
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Hypertension Fast Facts Series by Health Press, et al (2001); ISBN: 189954139X; http://www.amazon.com/exec/obidos/ASIN/189954139X/icongroupinterna
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Hypertension for the Clinician by J. Ian S. Robertson, Stephen G. Ball (Contributor); ISBN: 0702018120; http://www.amazon.com/exec/obidos/ASIN/0702018120/icongroupinterna
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Hypertension in Children and Adolescents by Giorgio Giovannrlli (1981); ISBN: 0890045232; http://www.amazon.com/exec/obidos/ASIN/0890045232/icongroupinterna
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Hypertension in Children: A Practical Approach by Leonard G. Feld; ISBN: 0750696788; http://www.amazon.com/exec/obidos/ASIN/0750696788/icongroupinterna
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Hypertension in Diabetes by Bryan Williams, Richard H. Williams; ISBN: 1853175528; http://www.amazon.com/exec/obidos/ASIN/1853175528/icongroupinterna
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Hypertension in Elderly People - pocketbook by Ken Woodhouse, Juanita Pascual (1996); ISBN: 185317324X; http://www.amazon.com/exec/obidos/ASIN/185317324X/icongroupinterna
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Hypertension in Focus by Pharmaceutical Press, Susan Shankie; ISBN: 0853694567; http://www.amazon.com/exec/obidos/ASIN/0853694567/icongroupinterna
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Hypertension in Kidney Disease (Developments in Nephrology, 14) by Jhoong, S. Cheigh, et al (1986); ISBN: 0898387973; http://www.amazon.com/exec/obidos/ASIN/0898387973/icongroupinterna
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Hypertension in Postmenopausal Women by Michel Safar, M. Stimpel (1994); ISBN: 0387581448; http://www.amazon.com/exec/obidos/ASIN/0387581448/icongroupinterna
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Hypertension in Postmenopausal Women by Franz H. Messerli (Editor), Franz C. Aepfelbacher (Editor) (1996); ISBN: 0824796527; http://www.amazon.com/exec/obidos/ASIN/0824796527/icongroupinterna
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Hypertension in Practice by D. Gareth Beevers MD FRCP, Graham A. MacGregor FRCP; ISBN: 1853170739; http://www.amazon.com/exec/obidos/ASIN/1853170739/icongroupinterna
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Hypertension in Practice; ISBN: 185317078X; http://www.amazon.com/exec/obidos/ASIN/185317078X/icongroupinterna
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Hypertension in Pregnancy by J. J. Walker (Editor), N. F. Gant (Editor); ISBN: 0412309106; http://www.amazon.com/exec/obidos/ASIN/0412309106/icongroupinterna
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Hypertension in Pregnancy by P. C. Rubin (Editor); ISBN: 0444504168; http://www.amazon.com/exec/obidos/ASIN/0444504168/icongroupinterna
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Hypertension in Pregnancy by David Churchill, D. Gareth Beevers; ISBN: 0727909207; http://www.amazon.com/exec/obidos/ASIN/0727909207/icongroupinterna
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Hypertension in Pregnancy by Michael A. Belfort (Editor), et al (2003); ISBN: 082470827X; http://www.amazon.com/exec/obidos/ASIN/082470827X/icongroupinterna
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Hypertension in Pregnancy: Proceedings of the Sixteenth Study Group of the Royal College of Obstetricians and Gynecologists (Reproductive and Perina) by F. Sharp,
Books 347
E.M. Symonds (Editor); ISBN: 0916859282; http://www.amazon.com/exec/obidos/ASIN/0916859282/icongroupinterna •
Hypertension in Primary Care: An International Symposium Held at Reykjavik, Iceland, April 1978 (Occasional Paper) by John Coope; ISBN: 0850840724; http://www.amazon.com/exec/obidos/ASIN/0850840724/icongroupinterna
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Hypertension in the Community (Bibliotheca Cardiologica, No 42) by Talma Rosenthal, Daonald S. Silverberg (Editor) (1987); ISBN: 3805545215; http://www.amazon.com/exec/obidos/ASIN/3805545215/icongroupinterna
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Hypertension in the Diabetic Patient: A Guide to Management by Ian McFarlane (2001); ISBN: 185009165X; http://www.amazon.com/exec/obidos/ASIN/185009165X/icongroupinterna
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Hypertension in the Dialyzed Patient: A Practical Guide by Belding H. Scribner (Editor) (2003); ISBN: 1402013558; http://www.amazon.com/exec/obidos/ASIN/1402013558/icongroupinterna
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Hypertension in the Elderly - Pocketbook by Norman M. Kaplan; ISBN: 1853177296; http://www.amazon.com/exec/obidos/ASIN/1853177296/icongroupinterna
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Hypertension in the Elderly (Clinical Hypertension and Vascular Disease) by Michael L., Md. Prisant (Editor) (2004); ISBN: 1588291979; http://www.amazon.com/exec/obidos/ASIN/1588291979/icongroupinterna
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Hypertension in the Elderly (Developments in Cardiovascular Medicine, 157) by Gastone Leonetti, Cesare Cuspidi (Editor) (1994); ISBN: 0792328523; http://www.amazon.com/exec/obidos/ASIN/0792328523/icongroupinterna
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Hypertension in the Elderly (Handbook of Hypertension) by A. Amery, J. Staessen (Editor); ISBN: 0444904719; http://www.amazon.com/exec/obidos/ASIN/0444904719/icongroupinterna
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Hypertension in the Older Adult by Andrew K. Scott (Editor); ISBN: 0340614757; http://www.amazon.com/exec/obidos/ASIN/0340614757/icongroupinterna
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Hypertension in the young and the old; ISBN: 0808913190; http://www.amazon.com/exec/obidos/ASIN/0808913190/icongroupinterna
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Hypertension in Women - pocketbook (1996); ISBN: 1853173401; http://www.amazon.com/exec/obidos/ASIN/1853173401/icongroupinterna
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Hypertension Management by Stephen N. Hunyor (Editor), Judith A. Whitworth (Editor); ISBN: 0864330529; http://www.amazon.com/exec/obidos/ASIN/0864330529/icongroupinterna
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Hypertension Management: Clinical Pathways, Guidelines, and Patient Education by Jo Gulledge (Editor), et al; ISBN: 0834217023; http://www.amazon.com/exec/obidos/ASIN/0834217023/icongroupinterna
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Hypertension Management: Clinical Practice and Therapeutic Dilemmas by Gary L. Wollam, W. Dallas Hall; ISBN: 0815140754; http://www.amazon.com/exec/obidos/ASIN/0815140754/icongroupinterna
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Hypertension manual: mechanisms, methods, management by John H. Laragh; ISBN: 0914316001; http://www.amazon.com/exec/obidos/ASIN/0914316001/icongroupinterna
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Hypertension Mechanisms by Irvine H. Page; ISBN: 0808917684; http://www.amazon.com/exec/obidos/ASIN/0808917684/icongroupinterna
348 Hypertension
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Hypertension Medicine by Michael A., Md. Weber (Editor); ISBN: 0896037886; http://www.amazon.com/exec/obidos/ASIN/0896037886/icongroupinterna
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Hypertension Primer: The Essentials of High Blood Pressure by Joseph L. Izzo (Editor), et al (1999); ISBN: 0683307061; http://www.amazon.com/exec/obidos/ASIN/0683307061/icongroupinterna
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Hypertension research : methods and models; ISBN: 0824713443; http://www.amazon.com/exec/obidos/ASIN/0824713443/icongroupinterna
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Hypertension Research: A Memoir: 1920-1960 by Irvine Heinly Page (1988); ISBN: 0080360793; http://www.amazon.com/exec/obidos/ASIN/0080360793/icongroupinterna
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Hypertension Secrets by Donald E. Hricik (Editor), et al; ISBN: 1560534710; http://www.amazon.com/exec/obidos/ASIN/1560534710/icongroupinterna
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Hypertension the Next Decade: Verapamil in Focus: Proceedings of an International Symposium, Berlin by A.A. Fleckenstein (Editor) (1987); ISBN: 0443039208; http://www.amazon.com/exec/obidos/ASIN/0443039208/icongroupinterna
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Hypertension Therapy Annual by Norman M. Kaplin (Editor), Norman M. Kaplan (Editor); ISBN: 1853177288; http://www.amazon.com/exec/obidos/ASIN/1853177288/icongroupinterna
•
Hypertension Therapy Annual 2002 by Norman Kaplan, Norman M. Kaplan; ISBN: 184184103X; http://www.amazon.com/exec/obidos/ASIN/184184103X/icongroupinterna
•
Hypertension Treatment: User Guide by Norman M. Kaplan (1993); ISBN: 0929240537; http://www.amazon.com/exec/obidos/ASIN/0929240537/icongroupinterna
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Hypertension, a Practical Approach by Murray Epstein, James Oster (1984); ISBN: 0721633978; http://www.amazon.com/exec/obidos/ASIN/0721633978/icongroupinterna
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Hypertension, Fluid-Electrolytes, and Tubulopathies in Pediatric Nephrology: Proceedings of Pediatric Nephrology Seminar Viii, Held in Bal Harbour, Florida, January 25-29, 1981 by Fla.)/ Strauss, Jose Pediatric Nephrology Seminar 1981 Bal Harbour, Strauss (Editor) (1982); ISBN: 9024726336; http://www.amazon.com/exec/obidos/ASIN/9024726336/icongroupinterna
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Hypertension, Mechanism, Diagnosis and Management: Mechanisms, Diagnosis, & Management by James O. Davis (Editor), et al; ISBN: 0913800074; http://www.amazon.com/exec/obidos/ASIN/0913800074/icongroupinterna
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Hypertension, Mechanisms & Clinical Aspects by Denny J. Meyer, Philippe Meyer (1992); ISBN: 0192612409; http://www.amazon.com/exec/obidos/ASIN/0192612409/icongroupinterna
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Hypertension, the renal basis; ISBN: 0879333561; http://www.amazon.com/exec/obidos/ASIN/0879333561/icongroupinterna
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Hypertension: A Clinician's Guide to Diagnosis and Treatment by Barry J., Md. Sobel, George L., M.D., Facp Bakris; ISBN: 1560533196; http://www.amazon.com/exec/obidos/ASIN/1560533196/icongroupinterna
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Hypertension: A Companion to Brenner & Rector's The Kidney by Suzanne Oparil (Editor), et al; ISBN: 0721677649; http://www.amazon.com/exec/obidos/ASIN/0721677649/icongroupinterna
Books 349
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Hypertension: A Guide to Assessment and Management with a History of Hypertension: A Guide to the Major Discoveries in Blood Circula by Neil Poulter, Michael Kirby (2002); ISBN: 1904218016; http://www.amazon.com/exec/obidos/ASIN/1904218016/icongroupinterna
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Hypertension: A Practical Approach by Brown, C1975.R Boston : Little; ISBN: 0316585408; http://www.amazon.com/exec/obidos/ASIN/0316585408/icongroupinterna
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Hypertension: An Atlas of Investigation and Diagnosis by Edward D. Frohlich (2004); ISBN: 1904392156; http://www.amazon.com/exec/obidos/ASIN/1904392156/icongroupinterna
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Hypertension: An Incredibly Easy! Miniguide (Incredibly Easy Miniguide,) by Springhouse Corporation, et al (1999); ISBN: 1582550107; http://www.amazon.com/exec/obidos/ASIN/1582550107/icongroupinterna
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Hypertension: Community Control of High Blood Pressure by Julian Tudor Hart; ISBN: 0443031525; http://www.amazon.com/exec/obidos/ASIN/0443031525/icongroupinterna
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Hypertension: Directory of Authors of New Medical and Scientific Reviews With Subject Index by Science, Life Consults (1995); ISBN: 0788305905; http://www.amazon.com/exec/obidos/ASIN/0788305905/icongroupinterna
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Hypertension: Diseases of the Aorta. by Larry Ward (Illustrator), et al (1994); ISBN: 1859226043; http://www.amazon.com/exec/obidos/ASIN/1859226043/icongroupinterna
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Hypertension: How to Work With Your Doctor and Take Charge of Your Health by Mike Samuels, Nancy Samuels (Contributor); ISBN: 0671682164; http://www.amazon.com/exec/obidos/ASIN/0671682164/icongroupinterna
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Hypertension: Human Plus (1997); ISBN: 1561020540; http://www.amazon.com/exec/obidos/ASIN/1561020540/icongroupinterna
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Hypertension: Mechanism, Diagnosis, and Treatment by Gaddo Onesti, Albert N. Brent (1978); ISBN: 0803666306; http://www.amazon.com/exec/obidos/ASIN/0803666306/icongroupinterna
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Hypertension: Mechanisms & Therapy by Norman K. Hollenberg (Editor), et al; ISBN: 1573401110; http://www.amazon.com/exec/obidos/ASIN/1573401110/icongroupinterna
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Hypertension: mechanisms and management; the twenty-sixth Hahnemann symposium; ISBN: 0808907905; http://www.amazon.com/exec/obidos/ASIN/0808907905/icongroupinterna
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Hypertension: Pathophysiology, Diagnosis, and Management by John H., M.D. Laragh, Barry M., M.D. Brenner (Editor) (1995); ISBN: 0781701570; http://www.amazon.com/exec/obidos/ASIN/0781701570/icongroupinterna
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Hypertension: Physiological Basis and Treatment by Helen H. Ong; ISBN: 0125268505; http://www.amazon.com/exec/obidos/ASIN/0125268505/icongroupinterna
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Hypertension: Practical Management by Murray Epstein, James R. Oster (1988); ISBN: 0961929502; http://www.amazon.com/exec/obidos/ASIN/0961929502/icongroupinterna
350 Hypertension
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Hypertension: Recent Advances and Research by Mario and Zanchetti, Alberto Condorelli (Editor) (1982); ISBN: 8885037380; http://www.amazon.com/exec/obidos/ASIN/8885037380/icongroupinterna
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Hypertension: The Nurse's Role in Ambulatory Care by New York :; ISBN: 0826123708; http://www.amazon.com/exec/obidos/ASIN/0826123708/icongroupinterna
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Hypertension: The Silent Killer by Luzano Pancho Canlas; ISBN: 0741408961; http://www.amazon.com/exec/obidos/ASIN/0741408961/icongroupinterna
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Hypertension: Your Questions Answered by Ian B. Wilkinson, et al (2003); ISBN: 0443072558; http://www.amazon.com/exec/obidos/ASIN/0443072558/icongroupinterna
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Hypertensive Disorders in Women by Baha M. MD Sibai (Editor), WB Saunders Company; ISBN: 0721673740; http://www.amazon.com/exec/obidos/ASIN/0721673740/icongroupinterna
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Hypertensive Disorders of Pregnancy (March of Dimes Nursing Modules) by Judith H. Poole, et al (1997); ISBN: 0865250774; http://www.amazon.com/exec/obidos/ASIN/0865250774/icongroupinterna
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Hypertensive Intracerebral Hemorrhage by Masahire Mizukami; ISBN: 0890048126; http://www.amazon.com/exec/obidos/ASIN/0890048126/icongroupinterna
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Idiopathic Portal Hypertension by Kunio Okuda (Editor); ISBN: 0860083535; http://www.amazon.com/exec/obidos/ASIN/0860083535/icongroupinterna
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Illustrated Multiple Choice Questions in Hypertension by Dallas Hall (1997); ISBN: 0723424780; http://www.amazon.com/exec/obidos/ASIN/0723424780/icongroupinterna
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Imaging and Hypertension (Saunders Monographs in Clinical Radiology, Vol 22) by Bruce J. Hillman; ISBN: 0721646786; http://www.amazon.com/exec/obidos/ASIN/0721646786/icongroupinterna
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Individualized Therapy of Hypertension by Norman M. Kaplan, C. Venkata S. Ram (Editor); ISBN: 0824792629; http://www.amazon.com/exec/obidos/ASIN/0824792629/icongroupinterna
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Inflammatory Vascular Diseases-Endo-Myocardial Fibrosis-Pulmonary Hypertension: Proceedings - Conference of the International Society of Geographical by J. R. Ruettner (Editor), International Society Of Geographical Pa (1976); ISBN: 3805523114; http://www.amazon.com/exec/obidos/ASIN/3805523114/icongroupinterna
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Inhalation Therapy for Pulmonary Hypertension: The Proceedings of a Symposium Held at the Annual Congress of the European Respiratory Society, Berlin, September 2001 by Timothy Higenbottam (Editor), et al (2002); ISBN: 1842141848; http://www.amazon.com/exec/obidos/ASIN/1842141848/icongroupinterna
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Introduction to the nature and management of hypertension by Edward D. Freis; ISBN: 0876180306; http://www.amazon.com/exec/obidos/ASIN/0876180306/icongroupinterna
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Investigation of Labetalol in the Management of Hypertension in Pregnancy by A. Riley; ISBN: 0444902724; http://www.amazon.com/exec/obidos/ASIN/0444902724/icongroupinterna
Books 351
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Ionic Transport in Hypertension New Perspectives by Antonio, M.D. Coca, Ricardo P., M.D. Garay (Editor); ISBN: 0849354749; http://www.amazon.com/exec/obidos/ASIN/0849354749/icongroupinterna
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Juvenile hypertension; ISBN: 0890041458; http://www.amazon.com/exec/obidos/ASIN/0890041458/icongroupinterna
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Kaplan's Clinical Hypertension by Norman M. Kaplan, et al; ISBN: 0781732247; http://www.amazon.com/exec/obidos/ASIN/0781732247/icongroupinterna
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Kidney and Hypertension by George Bakris; ISBN: 1841842702; http://www.amazon.com/exec/obidos/ASIN/1841842702/icongroupinterna
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Kidney in Essential Hypertension: Proceedings of the Course on the Kidney in Essential Hypertension, Held New Orleans, La, March 18-19, 1983 (Developments in Cardiovascular Medicine, V. 35.) by Course on the Kidney in Essential Hypertension (1983); ISBN: 0898386160; http://www.amazon.com/exec/obidos/ASIN/0898386160/icongroupinterna
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Kinins in blood and urine with special reference to intrarenal kinin formation in normal and hypertensive individuals by Lennart Hulthén; ISBN: 8774942085; http://www.amazon.com/exec/obidos/ASIN/8774942085/icongroupinterna
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Laragh's Lessons in Renin System Pathophysiology for Treating Hypertension and Its Fatal Cardiovascular Consequences by John H. Laragh; ISBN: 0080441343; http://www.amazon.com/exec/obidos/ASIN/0080441343/icongroupinterna
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Lebertumoren Und Portale Hypertension: Radiologische Und Chirurgische Aspekte by M. Reiser, et al (1993); ISBN: 038755999X; http://www.amazon.com/exec/obidos/ASIN/038755999X/icongroupinterna
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Lifelong Management of Hypertension (Developments in Cardiovascular Medicine, 26) by H. Mitchell Perry (Editor) (1983); ISBN: 0898385822; http://www.amazon.com/exec/obidos/ASIN/0898385822/icongroupinterna
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Lifestyle Modification for the Prevention and Treatment of Hypertension by Paul K. Whelton (Editor), et al; ISBN: 0824741188; http://www.amazon.com/exec/obidos/ASIN/0824741188/icongroupinterna
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Living With High Blood Pressure: The Hypertension Diet Cookbook by Joyce D. and Hunt, James C. Margie; ISBN: 0801968550; http://www.amazon.com/exec/obidos/ASIN/0801968550/icongroupinterna
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Low Dose Oral and Transdermal Therapy of Hypertension by M.A. Weber, et al (1985); ISBN: 0387912614; http://www.amazon.com/exec/obidos/ASIN/0387912614/icongroupinterna
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Major Problems in Clinical Pediatrics: Pediatric Hypertension by Julie R. Ingelfinger; ISBN: 072165021X; http://www.amazon.com/exec/obidos/ASIN/072165021X/icongroupinterna
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Management of essential hypertension by Francis Gilbert McMahon; ISBN: 0879931086; http://www.amazon.com/exec/obidos/ASIN/0879931086/icongroupinterna
•
Management of Essential Hypertension (1990); ISBN: 0879932147; http://www.amazon.com/exec/obidos/ASIN/0879932147/icongroupinterna
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Management of Hypertension by Norman M. Kaplan; ISBN: 0929240820; http://www.amazon.com/exec/obidos/ASIN/0929240820/icongroupinterna
352 Hypertension
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Management of Hypertension: A Multifactorial Approach by Norman K. Hollengerg (Editor) (1988); ISBN: 0936871040; http://www.amazon.com/exec/obidos/ASIN/0936871040/icongroupinterna
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Management of Renal Hypertension (New Clinical Applications: Nephrology) by G.R.D. Catto (Editor) (1989); ISBN: 0852006993; http://www.amazon.com/exec/obidos/ASIN/0852006993/icongroupinterna
•
Management of the Hypertensive Patient by Lawrence R. Krakoff (1995); ISBN: 0443087695; http://www.amazon.com/exec/obidos/ASIN/0443087695/icongroupinterna
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Managing Hypertension: The Complete Program Developed by the Cleveland Clinic (Frontiers of Medicine) by Genell Subak-Sharpe, James V. Warren; ISBN: 0385187688; http://www.amazon.com/exec/obidos/ASIN/0385187688/icongroupinterna
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Manual of Hypertension by Giuseppe, MD Mancia (Editor), et al; ISBN: 0443061955; http://www.amazon.com/exec/obidos/ASIN/0443061955/icongroupinterna
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Manual of Hypertension by J.D. Swales (Editor); ISBN: 0865428611; http://www.amazon.com/exec/obidos/ASIN/0865428611/icongroupinterna
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Manual of Nonpharmacological Control of Hypertension by J.R. Viskoper (Editor) (1990); ISBN: 0387510702; http://www.amazon.com/exec/obidos/ASIN/0387510702/icongroupinterna
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Mechanisms and Recent Advances in Therapy of Hypertension by H. Liebau (Editor) (1977); ISBN: 3805526717; http://www.amazon.com/exec/obidos/ASIN/3805526717/icongroupinterna
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Mechanisms in Hypertension: New Aspects in Hemodynamics by Lennart Hansson, Teruo Omae (Editor) (1989); ISBN: 0881675407; http://www.amazon.com/exec/obidos/ASIN/0881675407/icongroupinterna
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Medical and Surgical Aspects of Renovascular Hypertension: International Symposium, May 30-31, 1975, Gunzburg by Julian Rosenthal (1976); ISBN: 3805523416; http://www.amazon.com/exec/obidos/ASIN/3805523416/icongroupinterna
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Medical Management of Primary Hypertension by Lot B. Page; ISBN: 0316688193; http://www.amazon.com/exec/obidos/ASIN/0316688193/icongroupinterna
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Membrane Abnormalities in Hypertension by Chiu-Yin Kwan (Editor); ISBN: 0849345278; http://www.amazon.com/exec/obidos/ASIN/0849345278/icongroupinterna
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Metabolic Aspects of Hypertension by Norman M. Kaplan (Editor) (1994); ISBN: 1858730082; http://www.amazon.com/exec/obidos/ASIN/1858730082/icongroupinterna
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Mild Hypertension : Is There Pressure to Treat? by W. E. Miall (Author), Gillian Greenberg (Author); ISBN: 0521332931; http://www.amazon.com/exec/obidos/ASIN/0521332931/icongroupinterna
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Mild Hypertension: From Drug Trials to Practice by T. Strasser, Detlev Ganten (Editor) (1987); ISBN: 0881672475; http://www.amazon.com/exec/obidos/ASIN/0881672475/icongroupinterna
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Mild Hypertension: Recent Advances by Franz, Gross, Thomas Strasser (Editor); ISBN: 0890048088; http://www.amazon.com/exec/obidos/ASIN/0890048088/icongroupinterna
Books 353
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Mineralocorticoids and Hypertension by W. Kaufmann, G. Wambach; ISBN: 0387123911; http://www.amazon.com/exec/obidos/ASIN/0387123911/icongroupinterna
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Modern Approaches to the Treatment of Hypertension by L. I. Olbinskaya (Editor), et al (1976); ISBN: 3805524005; http://www.amazon.com/exec/obidos/ASIN/3805524005/icongroupinterna
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Modern Management of Renovascular Hypertension and Renal Salvage by Keith D. Calligaro (Editor), et al; ISBN: 0683013572; http://www.amazon.com/exec/obidos/ASIN/0683013572/icongroupinterna
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Molecular Genetics in Hypertension by Florent Soubrier (1999); ISBN: 0412130815; http://www.amazon.com/exec/obidos/ASIN/0412130815/icongroupinterna
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Molecular Genetics of Hypertension (A Volume in the Human Molecular Genetics Series) by A. F. Dominiczak (Editor), Florent Soubrier (Editor) (1999); ISBN: 0122204301; http://www.amazon.com/exec/obidos/ASIN/0122204301/icongroupinterna
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Morphological and morphormetrical analysis of circulation in hypertension and ischemic kidney by Norio Suwa; ISBN: 3541050519; http://www.amazon.com/exec/obidos/ASIN/3541050519/icongroupinterna
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Nephrology and Hypertension by C. Craig Tisher (Editor), Christopher S. Wilcox (Editor); ISBN: 078172077X; http://www.amazon.com/exec/obidos/ASIN/078172077X/icongroupinterna
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Neurogenic Hypertension (1991); ISBN: 0412396300; http://www.amazon.com/exec/obidos/ASIN/0412396300/icongroupinterna
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Neurogenic Hypertension: A Synthesis and Review by C.J. Dickinson (1991); ISBN: 0442314140; http://www.amazon.com/exec/obidos/ASIN/0442314140/icongroupinterna
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New Advances in Shr Research: Pathophysiology & Pharmacology (Progress in Hypertension, Vol 3) by H. Saito (Editor), et al (1995); ISBN: 9067641987; http://www.amazon.com/exec/obidos/ASIN/9067641987/icongroupinterna
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New Aspects in Hypertension: Adrenoceptors by M. Middeke, H. Holzgreve (Editor) (1986); ISBN: 0387168648; http://www.amazon.com/exec/obidos/ASIN/0387168648/icongroupinterna
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New Concepts in Pathogenesis and Treatment of Arterial Hypertension by Manvel Velasco (Editor), et al (1995); ISBN: 3437115707; http://www.amazon.com/exec/obidos/ASIN/3437115707/icongroupinterna
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New Perspectives on Hypertension by Adrian Brady, John Petrie; ISBN: 187341367X; http://www.amazon.com/exec/obidos/ASIN/187341367X/icongroupinterna
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New Therapeutic Strategies in Hypertension (Perspectives in Hypertension, Vol 3) by Norman M. Kaplan, et al (1989); ISBN: 0881675288; http://www.amazon.com/exec/obidos/ASIN/0881675288/icongroupinterna
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New Therapies for Pulmonary Arterial Hypertension: Orphan Drugs Seeking Opportunities in Wider Related Indications [DOWNLOAD: PDF] by Datamonitor (Author); ISBN: B00008R3WR; http://www.amazon.com/exec/obidos/ASIN/B00008R3WR/icongroupinterna
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New trends in arterial hypertension : proceedings of the Colloquium on New Trends in Arterial Hypertension--Cellular Pharmacology and Physiopathology held in
354 Hypertension
Deauville (France), 30 October - 1 November 1980; ISBN: 0444803246; http://www.amazon.com/exec/obidos/ASIN/0444803246/icongroupinterna •
NHLBI Workshop on Juvenile Hypertension : proceedings from a symposium, Bethesda, Maryland, May 26 and 27, 1983; ISBN: 0935404791; http://www.amazon.com/exec/obidos/ASIN/0935404791/icongroupinterna
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Non-Drug Treatments for Essential Hypertension (1988); ISBN: 0080328083; http://www.amazon.com/exec/obidos/ASIN/0080328083/icongroupinterna
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Non-Drug Treatments for Essential Hypertension (1988); ISBN: 0080328091; http://www.amazon.com/exec/obidos/ASIN/0080328091/icongroupinterna
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Non-Drug Treatments for Essential Hypertension (Psychology Practitioner Guidebooks Series) by Edward B. Blanchard; ISBN: 0205142869; http://www.amazon.com/exec/obidos/ASIN/0205142869/icongroupinterna
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Non-Pharmacologic Therapy of Hypertension (Bibliotheca Cardiologica, No 41) by M. Donald Blaufox, H. G. Langford (Editor) (1987); ISBN: 3805544596; http://www.amazon.com/exec/obidos/ASIN/3805544596/icongroupinterna
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Nutrition for Heart Disease and Hypertension; ISBN: 0572017200; http://www.amazon.com/exec/obidos/ASIN/0572017200/icongroupinterna
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Nutrition, Hypertension and Cardiovascular Disease by Ronald S. Smith (1989); ISBN: 0961422904; http://www.amazon.com/exec/obidos/ASIN/0961422904/icongroupinterna
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Nutritional Factors in Hypertension Section A: Selected Nutrients (Contemporary Issues in Clinical Nutrition) by Barbara Levine (Editor), et al; ISBN: 0471562335; http://www.amazon.com/exec/obidos/ASIN/0471562335/icongroupinterna
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Opioid Peptides and Blood Pressure Control: 11th Scientific Meeting of the International Society of Hypertension Satellite Symposium, Bonn, September 6-7, 1986 by K. Stumper (Editor), Et Al (Editor); ISBN: 3540189351; http://www.amazon.com/exec/obidos/ASIN/3540189351/icongroupinterna
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Over Coming Hypertension (Large Print) [LARGE PRINT] by T Cooper, Kenneth H. Cooper; ISBN: 038541577X; http://www.amazon.com/exec/obidos/ASIN/038541577X/icongroupinterna
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Overcoming Hypertension: Dr. Kenneth H. Cooper's Preventive Medicine Program (Dr. Kenneth H. Cooper's Preventive Medicine Program) by Kenneth H., M.D. Cooper; ISBN: 0553289373; http://www.amazon.com/exec/obidos/ASIN/0553289373/icongroupinterna
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Parois artérielles et hypertension expérimentale : implications dans la pathogénie de l'hypertension artérielle by Rorive Georges; ISBN: 2225415706; http://www.amazon.com/exec/obidos/ASIN/2225415706/icongroupinterna
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Pathology of Pulmonary Hypertension by Cornelis Adriaan. Wagenvoort; ISBN: 0471913553; http://www.amazon.com/exec/obidos/ASIN/0471913553/icongroupinterna
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Pathophysiology of Hypertension by Alberto Zanchetti (Editor), G. Mancia (Editor); ISBN: 0444825517; http://www.amazon.com/exec/obidos/ASIN/0444825517/icongroupinterna
Books 355
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Pathophysiology of Hypertension in Blacks (Clinical Physiology Series) by John C. S. Fray (Editor), Janice G. Douglas (Editor) (1992); ISBN: 0195067207; http://www.amazon.com/exec/obidos/ASIN/0195067207/icongroupinterna
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Patient Education Booklets: What You Should Know About Cardiovascular Disorders: Coronary Artery Disease/hyperlipidemia/heart Failure/hypertension (Patient Education Booklets) by J. Willis Hurst MD, et al; ISBN: 1563750244; http://www.amazon.com/exec/obidos/ASIN/1563750244/icongroupinterna
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Personality, Elevated Blood Pressure, and Essential Hypertension (Series in Health Psychology and Behavioral Medicine) by Ernest H. Johnson, et al (1992); ISBN: 1560321423; http://www.amazon.com/exec/obidos/ASIN/1560321423/icongroupinterna
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Pharmaceutical Management for Ambulatory Care - Hypertension Guideline [DOWNLOAD: PDF] by Apollo Managed Care Consultants (Author); ISBN: B0000713FP; http://www.amazon.com/exec/obidos/ASIN/B0000713FP/icongroupinterna
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Pharmacological and therapeutic aspects of hypertension by Austin Eric Doyle; ISBN: 0849353858; http://www.amazon.com/exec/obidos/ASIN/0849353858/icongroupinterna
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Pharmacological Profiles in Hypertension, Volume 1: Calcium Channel Blockers by Victor R. Preedy (Editor), H. Why (Editor); ISBN: 1841100307; http://www.amazon.com/exec/obidos/ASIN/1841100307/icongroupinterna
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Pharmacology and Management of Hypertension (Contemporary Issues in Nephrology, Vol 28) by William M. Bennett, David A. McCarron (Editor); ISBN: 0443088969; http://www.amazon.com/exec/obidos/ASIN/0443088969/icongroupinterna
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Pharmacology of Antihypertensive Drugs (Handbook of Hypertension, Vol 3) by P.A. Van Zwieten (Editor); ISBN: 0444903135; http://www.amazon.com/exec/obidos/ASIN/0444903135/icongroupinterna
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Pharmacotherapy of Renal Disease and Hypertension (Contemporary Issues in Nephrology Vol 17) by William M. Bennet, David A. McGarron (Editor) (1987); ISBN: 0443085412; http://www.amazon.com/exec/obidos/ASIN/0443085412/icongroupinterna
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Placental Glucocorticoid Barrier and Adult Hypertension (Medical Intelligence Unit) by C. R. W. Edwards (1998); ISBN: 0412116510; http://www.amazon.com/exec/obidos/ASIN/0412116510/icongroupinterna
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Pocket Picture Guide to Hypertension by J.D. Swales, P.S. Sever (Editor); ISBN: 0397448244; http://www.amazon.com/exec/obidos/ASIN/0397448244/icongroupinterna
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Portal Hypertension (1991); ISBN: 3350700544; http://www.amazon.com/exec/obidos/ASIN/3350700544/icongroupinterna
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Portal Hypertension II: Definitions, Methodology, and Therapeutic Strategies by Methodology, A Baveno International Consensus Workshop on Definitions, Roberto De Franchis (Editor) (1995); ISBN: 0865426147; http://www.amazon.com/exec/obidos/ASIN/0865426147/icongroupinterna
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Portal Hypertension III: Proceedings of the Third Baveno International Consensus Workshop on Definitions, Methodology, and Therapeutic Strategies by Methodology,
356 Hypertension
A Baveno International Consensus Workshop on Definitions, Roberto De Franchis (2001); ISBN: 0632059184; http://www.amazon.com/exec/obidos/ASIN/0632059184/icongroupinterna •
Portal Hypertension: A Multidisciplinary Approach to Current Clinical Management by Stuart J., Md. Knechtle (Editor); ISBN: 087993414X; http://www.amazon.com/exec/obidos/ASIN/087993414X/icongroupinterna
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Portal Hypertension: Clinical and Physiological Aspects by Kunio Okuda, Jean-Pierre Benhamou (Editor); ISBN: 0387700544; http://www.amazon.com/exec/obidos/ASIN/0387700544/icongroupinterna
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Portal Hypertension: Diagnostic Imaging and Imaging-Guided Therapy by Plinio Rossi (Editor), et al; ISBN: 3540657975; http://www.amazon.com/exec/obidos/ASIN/3540657975/icongroupinterna
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Portal Hypertension: Pathophysiology and Treatment by Jaime Bosch (Editor); ISBN: 0865428468; http://www.amazon.com/exec/obidos/ASIN/0865428468/icongroupinterna
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Practical Management of Hypertension (Developments in Cardiovascular Medicine, 184) by W. H. Birkenhager (Editor) (1996); ISBN: 0792339525; http://www.amazon.com/exec/obidos/ASIN/0792339525/icongroupinterna
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Practical Management of Hypertension in Diabetes by Neil Poulter, Bryan Williams (2003); ISBN: 1904218024; http://www.amazon.com/exec/obidos/ASIN/1904218024/icongroupinterna
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Pregnancy hypertension : a systematic evaluation of clinical diagnostic criteria by Emanuel A. Friedman; ISBN: 0884161854; http://www.amazon.com/exec/obidos/ASIN/0884161854/icongroupinterna
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Pregnancy Induced Hypertension by H.R. Seneviratne; ISBN: 0863118003; http://www.amazon.com/exec/obidos/ASIN/0863118003/icongroupinterna
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Preventing Hypertension by Herbert L. Langford; ISBN: 0875271855; http://www.amazon.com/exec/obidos/ASIN/0875271855/icongroupinterna
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Prevention of Atherosclerosis and Hypertension Beginning in Youth by Lloyd J., Jr., M.D. Filer, et al; ISBN: 0812116410; http://www.amazon.com/exec/obidos/ASIN/0812116410/icongroupinterna
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Primary Pulmonary Hypertension by Lewis J. Rubin (Editor), Stuart Rich (Editor) (1997); ISBN: 0824795059; http://www.amazon.com/exec/obidos/ASIN/0824795059/icongroupinterna
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Progress in Atrial Peptide Research (American Society of Hypertension Symposium Series, Vol 3) by Barry M. Brenner, John H. Laragh (Editor) (1989); ISBN: 0881675342; http://www.amazon.com/exec/obidos/ASIN/0881675342/icongroupinterna
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Progress in Clinical Kidney Disease and Hypertension by McDonald; ISBN: 0865771499; http://www.amazon.com/exec/obidos/ASIN/0865771499/icongroupinterna
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Progress in Clinical Kidney Disease and Hypertension (1985); ISBN: 3136619013; http://www.amazon.com/exec/obidos/ASIN/3136619013/icongroupinterna
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Progress in Hypertension: Neurotransmitters As Modulators of Blood Pressure (Vol 1) by H. Saito (Editor) (1987); ISBN: 9067641006; http://www.amazon.com/exec/obidos/ASIN/9067641006/icongroupinterna
Books 357
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Prostacyclin and Hypertension (1990); ISBN: 3540521402; http://www.amazon.com/exec/obidos/ASIN/3540521402/icongroupinterna
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Psychobiology of essential hypertension by Herbert Weiner; ISBN: 0444002758; http://www.amazon.com/exec/obidos/ASIN/0444002758/icongroupinterna
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Psychological Perspectives of Essential Hypertension: Etiology, Maintenance and Treatment by Wolfgang Linden (1984); ISBN: 3805536623; http://www.amazon.com/exec/obidos/ASIN/3805536623/icongroupinterna
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Psychology of Hypertension: Medical Analysis Index With Research Bibliography by Rosetta Roby. Hardine (1991); ISBN: 1559144602; http://www.amazon.com/exec/obidos/ASIN/1559144602/icongroupinterna
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Pulmonary Hypertension by Alfred P., Md. Fishman, Alfred P. Fishman M.D. ISBN: 0070220565; http://www.amazon.com/exec/obidos/ASIN/0070220565/icongroupinterna
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Pulmonary Hypertension: Proceedings of the International Symposium on Pulmonary Circulation II, Prague, June 17-19, 1974 by Jiri Widimsky (1975); ISBN: 3805521715; http://www.amazon.com/exec/obidos/ASIN/3805521715/icongroupinterna
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Renovascular and Renal Parenchymatous Hypertension (1992); ISBN: 3540533249; http://www.amazon.com/exec/obidos/ASIN/3540533249/icongroupinterna
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Renovascular Hypertension by James C. Stanley, et al; ISBN: 072168551X; http://www.amazon.com/exec/obidos/ASIN/072168551X/icongroupinterna
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Renovascular Hypertension by W. Vetter (Editor), et al (1986); ISBN: 3805543875; http://www.amazon.com/exec/obidos/ASIN/3805543875/icongroupinterna
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Renovascular Hypertension Chart by Anatomical Chart (2003); ISBN: 158779442X; http://www.amazon.com/exec/obidos/ASIN/158779442X/icongroupinterna
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Renovascular Hypertension: Pathophysiology, Diagnosis, and Treatment by Nicola Glorioso, et al (1987); ISBN: 0881672696; http://www.amazon.com/exec/obidos/ASIN/0881672696/icongroupinterna
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Reversing Hypertension: A Vital New Program to Prevent, Treat and Reduce High Blood. by Julian M.D. Whitaker (Author) (2001); ISBN: 0446676632; http://www.amazon.com/exec/obidos/ASIN/0446676632/icongroupinterna
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Risks Conveyed in Antihypertensive Treatment (1986); ISBN: 3437110365; http://www.amazon.com/exec/obidos/ASIN/3437110365/icongroupinterna
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Role of Endogenous Epinephrine in the Development of Experimental Hypertension (Soviet Medical Reviews Series, Section A) by O. S. Medvedev; ISBN: 371865234X; http://www.amazon.com/exec/obidos/ASIN/371865234X/icongroupinterna
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RXDX Training by Computer: Hypertension Management by Edward P. Hoffer, G. Octo Barnett (1998); ISBN: 0683404148; http://www.amazon.com/exec/obidos/ASIN/0683404148/icongroupinterna
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Salt and hypertension : proceedings of the Lewis K. Dahl Symposium; ISBN: 0896400727; http://www.amazon.com/exec/obidos/ASIN/0896400727/icongroupinterna
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Salt and Hypertension: Dietary Minerals, Volume Homeostasis and Cardiovascular Regulation; ISBN: 3540500634; http://www.amazon.com/exec/obidos/ASIN/3540500634/icongroupinterna
358 Hypertension
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Secondary forms of hypertension : current diagnosis and management : the second International Symposium of Nephrology, Montecatini, Italy, May 6-8, 1980; ISBN: 0808913840; http://www.amazon.com/exec/obidos/ASIN/0808913840/icongroupinterna
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Secondary Hypertension by H. Vetter (Editor) (1985); ISBN: 3805540795; http://www.amazon.com/exec/obidos/ASIN/3805540795/icongroupinterna
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Secondary Hypertension: Clinical Presentation Diagnosis, and Treatment (Clinical Hypertension and Vascular) by George A. Mansoor (Editor) (2004); ISBN: 1588291413; http://www.amazon.com/exec/obidos/ASIN/1588291413/icongroupinterna
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Shared Care for Hypertension by Poulter, et al; ISBN: 1899066802; http://www.amazon.com/exec/obidos/ASIN/1899066802/icongroupinterna
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Silent Disease: Hypertension by Lawrence Galton, Lawrence Gaiton; ISBN: 0451155130; http://www.amazon.com/exec/obidos/ASIN/0451155130/icongroupinterna
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Speaking of High Blood Pressure: A Comprehensive Guide for Hypertensives and Their Partners by Hanns Peter Wolff (1979); ISBN: 0832622354; http://www.amazon.com/exec/obidos/ASIN/0832622354/icongroupinterna
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Staff manual for teaching patients about hypertension by Betty Chewning; ISBN: 0872582515; http://www.amazon.com/exec/obidos/ASIN/0872582515/icongroupinterna
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Staff Manual for Teaching Patients About Hypertension 1982 Edition by Betty Chewning; ISBN: 0872584003; http://www.amazon.com/exec/obidos/ASIN/0872584003/icongroupinterna
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Stress and Hypertension by Symposium on Nephrology, et al; ISBN: 3805534507; http://www.amazon.com/exec/obidos/ASIN/3805534507/icongroupinterna
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Stress and Hypertension: MacRobiotic Health Education Series by Michio Kushi, Mark Mead (Editor); ISBN: 0870406787; http://www.amazon.com/exec/obidos/ASIN/0870406787/icongroupinterna
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Surgical management of systemic hypertension; ISBN: 0879931566; http://www.amazon.com/exec/obidos/ASIN/0879931566/icongroupinterna
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Systemic effects of antihypertensive agents : formal papers and selected edited discussions from the Effects of Antihypertensive Therapy Symposium; ISBN: 0883720485; http://www.amazon.com/exec/obidos/ASIN/0883720485/icongroupinterna
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Textbook of Hypertension by J.D. Swales (Editor); ISBN: 0632035277; http://www.amazon.com/exec/obidos/ASIN/0632035277/icongroupinterna
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The Adrenal and Hypertension: From Cloning to Clinic (Serono Symposia Publications, Vol 57) by F. Mantero, et al (1989); ISBN: 0881674214; http://www.amazon.com/exec/obidos/ASIN/0881674214/icongroupinterna
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The Arterial System in Hypertension (Developments in Cardiovascular Medicine, 144) by Michel Safar, Michael F. O'Rourke (Editor) (1993); ISBN: 0792323432; http://www.amazon.com/exec/obidos/ASIN/0792323432/icongroupinterna
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The Biochemistry of Hypertension by J. Rosenthal, et al (1988); ISBN: 3805548494; http://www.amazon.com/exec/obidos/ASIN/3805548494/icongroupinterna
Books 359
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The Black Health Library Guide to Heart Disease and Hypertension (Black Health Library) by Marcelo Oliver (Illustrator), et al; ISBN: 0805022678; http://www.amazon.com/exec/obidos/ASIN/0805022678/icongroupinterna
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The Calcium Connection: A Revolutionary Diet and Health Program to Reduce Hypertension, Prevent Osteoporosis, and Lower the Risk of Cancer by Cedric Garland, et al; ISBN: 0671671928; http://www.amazon.com/exec/obidos/ASIN/0671671928/icongroupinterna
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The Calcium Connection: A Revolutionary Diet and Health Program to Reduce Hypertension, Prevent Osteoporsis, and Lower the Risk of Cancer by Cedric Garland; ISBN: 0399132929; http://www.amazon.com/exec/obidos/ASIN/0399132929/icongroupinterna
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The Causes of Hypertension: Integrative Circulatory Control by Paul I. Korner (2003); ISBN: 0195094832; http://www.amazon.com/exec/obidos/ASIN/0195094832/icongroupinterna
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The DASH Diet for Hypertension by Thomas J. Moore (Editor), et al; ISBN: 0743410076; http://www.amazon.com/exec/obidos/ASIN/0743410076/icongroupinterna
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The Heart and Hypertension by Franz H. Messerli (Editor); ISBN: 0914316451; http://www.amazon.com/exec/obidos/ASIN/0914316451/icongroupinterna
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The Heart in Hypertension: A Tribute to Robert Tarazi by M.E. Safar, et al (1990); ISBN: 0792301978; http://www.amazon.com/exec/obidos/ASIN/0792301978/icongroupinterna
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The hypertension handbook. by Merck Sharp & Dohme (Author), National High Blood Pressure Education Program (Author); ISBN: 0911910220; http://www.amazon.com/exec/obidos/ASIN/0911910220/icongroupinterna
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The Hypertension Report: Say Goodbye to High Blood Pressure by William Campbell Douglass (2003); ISBN: 9962636604; http://www.amazon.com/exec/obidos/ASIN/9962636604/icongroupinterna
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The Hypertension Sourcebook by Mary P., Md. McGowan, Jo McGowan-Chopra; ISBN: 0737305398; http://www.amazon.com/exec/obidos/ASIN/0737305398/icongroupinterna
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The Hypertensive patient; ISBN: 0839114664; http://www.amazon.com/exec/obidos/ASIN/0839114664/icongroupinterna
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The Johns Hopkins White Papers 2002, Volume 2: Hypertension and Stroke, Low Back Pain and Osteoporosis, Memory, Prostate Disorders, Vision by Simeon Margolis (Editor) (2002); ISBN: 0929661729; http://www.amazon.com/exec/obidos/ASIN/0929661729/icongroupinterna
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The Johns Hopkins White Papers: Hypertension and Stroke by Lawrence Appel, et al; ISBN: 0929661567; http://www.amazon.com/exec/obidos/ASIN/0929661567/icongroupinterna
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The Kidney and Hypertension in Diabetes Mellitus by Carl Erik Mogensen (Editor), Anna Honore (Editor); ISBN: 0792379012; http://www.amazon.com/exec/obidos/ASIN/0792379012/icongroupinterna
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The Kidney in Hypertension (Perspectives in Hypertension, Vol 1) by Norman M. Kaplan, et al (1987); ISBN: 088167298X; http://www.amazon.com/exec/obidos/ASIN/088167298X/icongroupinterna
360 Hypertension
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The Metabolic Syndrome X: Convergence of Insulin Resistance, Glucose Intolerance, Hypertension, Obesity, and Dyslipidemias-Searching for the Underlying Defeats (Annals of the New York Academy of Sciences (Cloth), Vol 892) by Barbara Caleen Hansen (Editor), et al; ISBN: 157331207X; http://www.amazon.com/exec/obidos/ASIN/157331207X/icongroupinterna
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The nervous system in arterial hypertension : [proceedings]; ISBN: 0398033773; http://www.amazon.com/exec/obidos/ASIN/0398033773/icongroupinterna
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The Official Patient's Sourcebook on Primary Pulmonary Hypertension by Icon Health Publications, et al (2002); ISBN: 0597831548; http://www.amazon.com/exec/obidos/ASIN/0597831548/icongroupinterna
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The Renal papilla and hypertension; ISBN: 0306405067; http://www.amazon.com/exec/obidos/ASIN/0306405067/icongroupinterna
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The Role of Salt in Cardiovascular Hypertension by Melvin Fregly; ISBN: 0122672801; http://www.amazon.com/exec/obidos/ASIN/0122672801/icongroupinterna
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The Sympathetic Nervous System and Hypertension - pocketbook by Michael Schachter; ISBN: 1853174262; http://www.amazon.com/exec/obidos/ASIN/1853174262/icongroupinterna
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The treatment of hypertension; ISBN: 0839113161; http://www.amazon.com/exec/obidos/ASIN/0839113161/icongroupinterna
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The Year in Hypertension 2000 by Professor J. M. C. Connell, et al; ISBN: 0953733904; http://www.amazon.com/exec/obidos/ASIN/0953733904/icongroupinterna
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The Year in Hypertension 2001 by J.M.C. Connell, et al; ISBN: 0953733947; http://www.amazon.com/exec/obidos/ASIN/0953733947/icongroupinterna
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The Yearbook of Nephrology, Hypertension, and Mineral Metabolism 1999 by Steve J. Schwab (Editor), et al (1999); ISBN: 0815196474; http://www.amazon.com/exec/obidos/ASIN/0815196474/icongroupinterna
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Theories and use of gb s-blockade in hypertension and angina : an international symposium; ISBN: 0883721228; http://www.amazon.com/exec/obidos/ASIN/0883721228/icongroupinterna
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Therapy of Nephrology and Hypertension: A Companion to Brenner and Rector's the Kidney by Hugh R. Brady (Editor), Christopher S. Wilcox (Editor) (2003); ISBN: 0721696813; http://www.amazon.com/exec/obidos/ASIN/0721696813/icongroupinterna
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Topics in hypertension; ISBN: 0914316206; http://www.amazon.com/exec/obidos/ASIN/0914316206/icongroupinterna
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Topics in Pathophysiology of Hypertension (Developments in Cardiovascular Medicine) by Herman Villarreal (Editor), Mohinder P. Sambhi (Editor) (1983); ISBN: 0898385954; http://www.amazon.com/exec/obidos/ASIN/0898385954/icongroupinterna
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Treatment of Hypertension in Primary Care - pocketbook by Norman M. Kaplan (2000); ISBN: 185317906X; http://www.amazon.com/exec/obidos/ASIN/185317906X/icongroupinterna
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Treatment of Hypertension With Urapidil: Preclinical and Clinical Update (International Congress and Symposium Series, No 101) by A. Amery (Editor) (1987);
Books 361
ISBN: 0905958292; http://www.amazon.com/exec/obidos/ASIN/0905958292/icongroupinterna •
Treatment of Pulmonary Hypertension by Inhaled Delivery: International Symposium on Pulmonary Circulation Vii, Wednesday 30 Kune 1999, Prague, Czech Republic by Czechos International Symposium on Pulmonary Circulation 1999 Prague, et al (2000); ISBN: 1842140809; http://www.amazon.com/exec/obidos/ASIN/1842140809/icongroupinterna
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Understanding and Managing Hypertension: The Reliable Healthcare Companions by John L. Decker, Harry R. Keiser (Editor); ISBN: 0380752484; http://www.amazon.com/exec/obidos/ASIN/0380752484/icongroupinterna
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Understanding Hypertension: Causes and Treatments by Medical Library Home, Timothy N. Caris; ISBN: 0446340790; http://www.amazon.com/exec/obidos/ASIN/0446340790/icongroupinterna
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Variability of Blood Pressure and Heart Rate in Borderline and Mild Hypertension: With Special Reference to Spectral Analysis (Comprehensive Summaries of Uppsala Dissertations, 854) by Reijo Takalo (1999); ISBN: 915544508X; http://www.amazon.com/exec/obidos/ASIN/915544508X/icongroupinterna
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Vasodepressor Hormones in Hypertension Prostaglandins and Kallikrein-Kinins (1988); ISBN: 3764319224; http://www.amazon.com/exec/obidos/ASIN/3764319224/icongroupinterna
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Vasodilatation and Beta-blockade: a New Standard in Hypertension? (International Congress and Symposium Series (ICSS)) by P.A. Van Zwieten (Editor); ISBN: 1853151955; http://www.amazon.com/exec/obidos/ASIN/1853151955/icongroupinterna
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Very-low-dose Combination Therapy in Hypertension by A. Pessina; ISBN: 1858739772; http://www.amazon.com/exec/obidos/ASIN/1858739772/icongroupinterna
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What Your Doctor May Not Tell You About Hypertension: The Revolutionary Nutrition. by Mark C. Houston, et al (2003); ISBN: 0446690848; http://www.amazon.com/exec/obidos/ASIN/0446690848/icongroupinterna
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Working Group Report on Hypertension in the Elderly by Henry R. Black, et al (1994); ISBN: 0788141678; http://www.amazon.com/exec/obidos/ASIN/0788141678/icongroupinterna
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Working Group Report on Primary Prevention of Hypertension: National High Blood Pressure Education Program by Edward J. Roccella (1993); ISBN: 0788142267; http://www.amazon.com/exec/obidos/ASIN/0788142267/icongroupinterna
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Year in Hypertension 2003 by Gregory Y. H. Lip, Wai K. Lee (2003); ISBN: 190439213X; http://www.amazon.com/exec/obidos/ASIN/190439213X/icongroupinterna
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Yearbook of Nephrology Hypertension and Mineral Metabolism 1998 by Steve J. Schwab (Editor), et al (1998); ISBN: 0815196466; http://www.amazon.com/exec/obidos/ASIN/0815196466/icongroupinterna
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Yoga on Hypertension by Shankardevananda S. (1998); ISBN: 8185787271; http://www.amazon.com/exec/obidos/ASIN/8185787271/icongroupinterna
362 Hypertension
The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “hypertension” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 •
Antihypertensive therapy, principles and practice; an international symposium. Proceedings, ed. by F. Gross with the assistance of S. R. Naegeli and A. H. Kirkwood. Author: Gross, F. H. (Franz Heinrich); Year: 1962; New York, Springer, 1966
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Baroreceptors and hypertension; proceedings of an international symposium held at Dayton, Ohio, 16-17 November 1965. Edited by P. Kezdi. Author: Kezdi, Paul,; Year: 1965; Oxford, New York, Symposium Publications Division, Pergamon Press [1967]
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Drug treatment of hypertension. Author: Page, Irvine H. (Irvine Heinly),; Year: 1962; [Siena, Ciba, 1965?]
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Electric sleep therapy of hypertension. Author: Sergeev, Georgii Vasil'evich.; Year: 1964; Washington, U. S. Joint Publications Research Service, 1966, reprinted 1967
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Health care guideline: hypertension diagnosis and treatment Author: Institute for Clinical Systems Improvement.; Year: 2003; [Bloomington, Minn.]: ICSI, c2003
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Hormones and hypertension. Author: Manger, William Muir,; Year: 2000; Springfield, Ill., Thomas [c1966]
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Hypertension and hypertensive heart disease in adults, United States, 1960-1962. A discussion of the criteria used for the diagnosis of hypertension and hypertensive heart disease, with data on the prevalence of hypertension and hypertensive heart disease by age, sex, and race, and an analysis of differentials by place, family income, education, marital status, usual activity, occupation, and industry. Author: National Center for Health Statistics (U.S.); Year: 1965; Washington, 1966
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Hypertensive vascular disease; diagnosis and treatment [by] Marvin Moser and Arthur G. Goldman. Author: Moser, Marvin,; Year: 2004; Philadelphia, Lippincott [c1967]
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Morphologic and functional contributions to the knowledge of arterial hypertension. Transactions of the symposium presented in the annual scientific meeting of the Society of Pathologists of Puerto Rico, February 24 to 29, 1964. Author: Costero, Isaac.; Year: 1962; [San Juan] Univ. of Puerto Rico. [1965]
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Morphologic and functional contributions to the knowledge of arterial hypertension: transactions of the symposium presented in the annual scientific meeting of the Society of Pathologists of Puerto Rico, February 24 to 29, 1964. Editor: Isaac Costero. Author: Costero, Isaac.; Year: 1962; San Juan] Univ. of Puerto Rico [1966. c1965]
11
In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.
Books 363
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Neurogenic hypertension. Author: Dickinson, C. J. (Christopher John); Year: 1962; Oxford, Blackwell [c1965]
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Pathology and treatment of hypertension. Author: Medimpex (Firm); Year: 1962; Budapest, Scientific Dept., Medimpex [1965]
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Portal hypertension [by] Cornelius E. Sedgwick [and] John K. Poulantzas. Author: Sedgwick, Cornelius E.,; Year: 1965; Boston, Little, Brown [c1967]
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Portal hypertension. Author: Longmire, William P.; Year: 2001; Chicago, Year Book Medical Publishers, 1966
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Primary pulmonary hypertension. Author: Walcott, George,; Year: 1966; [Minneapolis] 1967
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Renal hypertension. Edited by Irvine H. Page and James W. McCubbin. Author: Page, Irvine H. (Irvine Heinly),; Year: 1962; Chicago, Yearbook Medical Publishers [c1968]
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Serum cholesterol, parental longevity, overweight, and hypertension in the old; a factorial study by Anni Seppänen [et al.]. Author: Seppänen, Anni.; Year: 1963; Helsinki, 1963
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The Epidemiology of hypertension; proceedings of an international symposium.Chicago, Illinois, February 3-7, 1964. [Edited by] Jeremiah Stamler [et al.]. Author: Stamler, Jeremiah,; Year: 1959; New York, London, Grune; Stratton, 1967
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The therapy of portal hypertension; proceedings, Verhandlungen, comptes rendus. Edited by Nicola G. Markoff. Author: Markoff, Nicola G.; Year: 1962; Stuttgart, Thieme, 1968
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The William Fordham's first memorial lecture on the therapy of arteriosclerosis and essential hypertension by activation of fibrinolysis and facts that put this on a pharmacologic basis. Author: Misirlioglu, Yusuf Izzettin.; Year: 2002; Brooklyn, Dept. of Surgery, Unity Hospital, 1964
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Three views of hypertension and heart disease; examination diagnoses of hypertension and heart disease made in the first cycle of the Health Examination Survey are compared with reports of these diseases on a self-administered medical history and on an inquiry completed by the person's own physician. Author: National Center for Health Statistics (U.S.); Year: 1963; Washington [For sale by the Superintendent of Documents, U. S. Govt. Print. Off.] 1967
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Treatment of hypertension; guest editor: Alvin P. Shapiro. Treatment of pituitary disorders; guest editor: Raymond V. Randall. Author: Shapiro, Alvin P. (Alvin Philip),; Year: 1961; [New York] Hoeber, 1966
Chapters on Hypertension In order to find chapters that specifically relate to hypertension, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and hypertension using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “hypertension” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on hypertension:
364 Hypertension
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Hypertension in Dialysis Patients Source: in Lameire, N. and Mehta, R.L., eds. Complications of Dialysis. New York, NY: Marcel Dekker, Inc. 2000. p. 471-484. Contact: Available from Marcel Dekker, Inc. Cimarron Road, P.O. Box 5005, Monticello, NY 12701. (800) 228-1160 or (845) 796-1919. Fax (845) 796-1772. E-mail:
[email protected]. International E-mail:
[email protected]. Website: www.dekker.com. PRICE: $250.00 plus shipping and handling. ISBN: 0824788710. Summary: Arterial hypertension (high blood pressure) remains one of the major public health problems of industrialized nations, resulting in a great burden of morbidity (illness), mortality (death), and cost. For patients with end stage renal disease (ESRD), hypertension poses a particular problem, notably contribution to the high rates of cardiovascular disease and mortality experienced by dialysis patients. This chapter on hypertension in hemodialysis (HD) and peritoneal dialysis (PD) patients is from a book that offers a comprehensive, multidisciplinary resource for the nephrologist and caregiver providing dialysis, covering all aspects of dialysis therapies and their complications. In this chapter, the authors review the complicated subject of hypertension management for patients treated with HD or PD. The authors cover the measurement of blood pressure in dialysis patients; target blood pressure values; pathogenesis; the role of sodium and volume excess and the renin angiotensin axis; sympathetic activity; the role of erythropoietin; the role of divalent ions and parathyroid hormone; the vascular endothelium; and outcomes and treatment of hypertension in dialysis patients. Nonmedicinal treatments of hypertension can include aerobic exercise, control of salt and fluid intake, cessation of smoking, weight reduction, and avoidance of alcohol. The authors stress that the approach to the control of hypertension in dialysis patients should be multidisciplinary (medical, nursing, social work, and dietary). The mainstay of therapy for the control of hypertension in dialysis patients is adequate fluid removal. The use of antihypertensive medications is summarized in table format. 7 tables. 127 references.
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Effects of Hypertension on the Kidney Source: in Schena, F.P., ed. Nephrology. New York, NY: McGraw-Hill, Inc. 2001. p. 349354. Contact: Available from McGraw-Hill, Inc. Shoppenhangers Road, Maidenhead, Berkshire SL6 2QL. 44 (0)1628 502700. Fax: +44 (0)1628 635895 E-mail:
[email protected]. Website: www.mcgraw-hill.co.uk. PRICE: $79.95; plus shipping and handling. ISBN: 0077095251. Summary: Hypertension (high blood pressure) can cause renal (kidney) damage through two main mechanisms: those that involve the direct transmission of systemic hypertension to the body of the kidney and those that act indirectly on the kidney by inducing stenosis (narrowing of blood vessels) or occlusion (blockage) of preglomerular vessels and, in turn, ischemia (lack of blood flow) of the kidney. This chapter on the effects of hypertension on the kidney is from a book on nephrology (the study of the kidney and kidney diseases) designed for general practitioners and family care providers that offers strategies for the management of patients with renal (kidney) damage. Glomerular hypertension (high blood pressure in the capillaries of the filtering units of the kidney) may be present in diabetes mellitus, in primary renal diseases, and when renal mass is reduced. Elevated proteinuria (levels of protein in the urine) is the clinical sign of glomerular hypertension. On the other hand, patients with preglomerular vessel changes (such as stenosis) present a different clinical picture. The
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authors stress that the correct identification of the pathogenetic pathways (how the disease is developing) may help the practitioner to tailor the best treatment for his or her patients. In patients with glomerular hypertension, very strict control of blood pressure is mandatory, preferably with ACE inhibitors. In patients with preglomerular vessel changes, hypertension should be treated, but a careful control of serum creatinine is also mandatory, particularly when ACE inhibitors are used. Because kidney ischemia, not hypertensive stress, is the real problem, excessive reduction in blood pressure can harm the kidney organ. In these patients, the treatment of choice (when possible) is renal revascularization (surgery to bring additional blood vessels to the kidney). A patient care algorithm is provided. 1 figure. 2 tables. 15 references. •
Portal Hypertension-1: Varices Source: in Beckingham, I.J., ed. ABC of Liver, Pancreas and Gallbladder. London, UK: BMJ Publishing Group. 2001. p.18-21. Contact: Available from BMJ Publishing Group. BMA Books, BMA House, Tavistock Square, London WCIH 9JR. Fax 44 (0)20 7383 6402. E-mail:
[email protected]. Website: www.bmjbooks.com. PRICE: Contact publisher for price. ISBN: 0727915312. Summary: Portal hypertension is abnormally increased blood pressure in the portal venous system; it is a frequent complication of cirrhosis (scarring) of the liver. Varices are enlarged blood or lymphatic vessels. This chapter on portal hypertension and the role of varices is from an atlas of the liver, pancreas and gallbladder. The authors caution that variceal bleeding is the most serious complication and is an important cause of death in patients with cirrhotic liver disease. Topics covered include the diagnosis of varices, initial measures, and pharmacological control of varices; the use of emergency endoscopy, including sclerotherapy, band ligation, and the balloon tube tamponade; alternative management with the transjugular intrahepatic portosystemic shunt; long term management, including repeated endoscopic treatment, long term drug treatment and surgical procedures; prophylactic management; and the problem of gastric (stomach) varices and portal hypertensive gastropathy. The chapter concludes with summary points of the concepts discussed. 8 figures. 3 tables. 3 references.
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Preeclampsia in Pregnant Women with Chronic Hypertension and Renal Disease Source: Belfort, M.A. Thornton, S. Saade, G.R., eds. Hypertension in Pregnancy. Monticello, NY: Marcel Dekker, Inc. 2003. p.117-139. Contact: Available from Marcel Dekker, Inc. P.O. Box 5005, Monticello, NY 12701-5185. (800) 228-1160 or (212) 696-9000. Fax (845) 796-1772. E-mail:
[email protected]. Website: www.dekker.com. ISBN: 082470827X. PRICE: $000.00 plus shipping and handling. Summary: Preeclampsia (acute hypertension, proteinuria, and edema) is an important cause of maternal and fetal morbidity (complications) and mortality (death), complicating 5 to 10 percent of all pregnancies. This chapter on preeclampsia in pregnant women with chronic hypertension and renal (kidney) disease is from a textbook on hypertension (high blood pressure) in pregnancy. The authors note that there are major diagnostic difficulties in distinguishing preeclampsia, chronic hypertension, renal disease, and combinations of these separate entities. The chapter focuses on defining hypertension in pregnancy in relation to preexisting pathology, identifying the pitfalls in the detection and diagnosis of preeclampsia in women with chronic hypertension or renal disease (or both), and highlighting the controversies
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surrounding the prenatal care and obstetric problems in these women. 1 figure. 7 tables. 104 references. •
Portal Hypertension in Patients with Primary Biliary Cirrrhosis Source: in Lindor, K.D. Heathcote, E.J. Poupon, R., eds. Primary Biliary Cirrhosis: From Pathogenesis to Clinical Treatment. Boston, MA: Kluwer Academic Publishers. 1998. p. 87-91. Contact: Available from Kluwer Academic Publishers. Customer Service Deparment, P.O. Box 358, Accord Station, Hingham, MA 02018-0358. (781) 871-6600. Fax (781) 6819045. E-mail:
[email protected]. Website: www.wkap.nl. Summary: Primary biliary cirrhosis (PBC) is a chronic cholestasic (lack of bile flow) liver disease of unknown etiology (cause), although the association with a large number of autoimmune disorders suggests that the disease may be of autoimmune origin. The disease usually affects middle aged women and progresses from asymptomatic disease with only laboratory abnormalities to a severe cholestatic disease with deep jaundice, xanthomas (fatty tumors in the skin), portal hypertension (high blood pressure), and eventually liver failure. This chapter on portal hypertension (high blood pressure) is from a monograph that reprints papers from a conference held in November 1997 in Chicago, Illinois, on the clinical features (symptoms), pathogenesis, and treatment of PBC. Portal hypertension can result in the development of esophageal and gastric varices (enlarged veins or arteries) that, when of a large size, may bleed. Portal hypertension is increased venous pressure in the pathway of blood flow from the gastrointestinal tract and spleen to the liver; it is caused by compression or occlusion (blockage). The authors note that portal hypertension is not an uncommon finding in patients referred for the initial diagnosis of PBC, but it is also rarely severe. In patients not treated with UDCA (ursodeoxycholic acid), a progressive and slowly developing portal hypertension appears to occur with time. In patients treated with UDCA, progression of portal hypertension can be slowed during the first 2 years of treatment and, eventually, can be reversed after prolonged treatment. 8 references.
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Hypertension in Progressive Renal Disease Source: in Koch, K.M. and Stein, G., eds. Pathogenetic and Therapeutic Aspects of Chronic Renal Failure. New York, NY: Marcel Dekker, Inc. 1997. p. 13-19. Contact: Available from Marcel Dekker, Inc. 270 Madison Avenue, New York, NY 10016. (212) 696-9000. Fax (212) 685-4540. PRICE: $115.00. ISBN: 0824798945. Summary: The regulation of blood pressure (BP) and the function of the kidney are closely related. Renal disease may cause high BP and high BP may damage the kidneys, setting the scenario for a vicious cycle. Nephrologists are specifically concerned about the fact that hypertension may worsen the prognosis of chronic renal disease and may even damage previously healthy kidneys. This chapter on hypertension in progressive renal disease is from a book based on an international workshop, Chronic Renal Failure: Pathogenetic and Therapeutic Aspects, held in Berlin in May 1996. The authors review how chronically elevated, nonmalignant arterial BP may affect the natural course of chronic renal diseases. The authors also review studies that investigated how antihypertensive treatment affects progressive renal insufficiency. Positive data from large, prospective, double-blind studies are available only for ACE inhibitors; the renal benefit of ACE inhibition was apparent in both relatively mild and moderate chronic renal failure. In addition, the data suggest that the earlier treatment is started, the greater the benefit. The authors consider issues of safety and toxicity of ACE inhibitors.
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In addition, several ACE inhibitors have been shown to reduce cardiac mortality in patients at risk and possibly to lower the rate of myocardial reinfarctions. 15 references. •
Hypertension and Medical Nutrition Therapy Source: in Franz, M.J. and Bantle, J.P., eds. American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes. Alexandria, VA: American Diabetes Association. 1999. p. 295-311. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $39.95 for members; $49.95 for nonmembers; plus shipping and handling. ISBN: 158040006X. Order number 561601. Summary: This chapter focuses on the use of medical nutrition therapy (MNT) in treating hypertension in people with diabetes and presents the recommendations issued by the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Numerous randomized, controlled clinical trials have provided strong evidence that lowering blood pressure reduces renal and other complications of diabetes. In the United Kingdom Prospective Diabetes Study, angiotensin converting enzyme (ACE) inhibitors and beta blockers were equally effective and beneficial in treating hypertension. ACE inhibitors may be preferable if albuminuria is present because they are renoprotective and because recent evidence suggests that they may also be cardioprotective. The final results of the Appropriate Blood Pressure Control in Diabetes Trial will provide evidence to judge the best medical treatment approach for individuals who have diabetes and hypertension. Extrapolating from more general studies, weight reduction appears to be the preferable treatment for hypertension in people who have diabetes. Although sodium restriction appears to be effective in lowering blood pressure in sodium sensitive people, severe sodium restriction can worsen lipids and insulin resistance, and present a possible cardiovascular risk. There is no evidence to support the supplemental use of fish oils, potassium, or calcium. The Dietary Approaches To Stop Hypertension Trial demonstrated that a diet high in fruits and vegetables, low in total and saturated fats and cholesterol, and high in whole grains, as well as being moderately low in sodium lowered blood pressure. 5 tables. 36 references.
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Nutrition Counseling in Treatment of Hypertension Source: in Snetselaar, L.G. Nutrition Counseling Skills for Medical Nutrition Therapy. Gaithersburg, MD: Aspen Publishers, Inc. 1997. p. 310-336. Contact: Available from Aspen Publishers, Inc. Fulfillment, 7201 McKinney Circle, Frederick, MD 21704. (800) 234-1660 or (800) 638-8437. PRICE: $55.00. ISBN: 0834207559. Summary: This chapter is from a textbook that focuses on increasing the effectiveness of nutrition counselors as facilitators of behavioral change. The author uses the term 'nutrition counselor' to describe all health professionals involved in counseling clients or patients to provide dietary information or facilitate dietary adherence. This chapter discusses the use of nutrition counseling in the treatment of hypertension. Topics include inappropriate eating behaviors associated with sodium-modified regimens (low-salt diets); the assessment of a baseline diet for clients requiring a sodium-modified eating pattern; strategies to treat inappropriate eating behaviors; theories and facts about nutrition and hypertension; and dietary adherence tools for clients following sodium-modified eating plans. The tools include a handout on spices for low-sodium diets, a handout noting the estimated natural sodium content of foods, and a daily food
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record that provides an emphasis on sodium intake (the latter can be used as a monitoring device). 3 appendices. 6 tables. 88 references. (AA-M). •
Cardiovascular Risk Reduction in Hypertensive Diabetics Source: in Moser, M. and Sowers, J.R. Clinical Management of Cardiovascular Risk Factors in Diabetes. Caddo, OK: Professional Communications, Inc. 2002. p.119-149. Contact: Available from Professional Communications, Inc., Fulfillment Center, PO Box 10, Caddo, OK 74729-0010. (800)337-9838. Fax (580)367-9989. E-mail:
[email protected]. ISBN: 1884735665. PRICE: $21.95, plus shipping and handling. Summary: This chapter on cardiovascular risk reduction in patients with hypertension and diabetes is from a handbook that offers a concise overview of the clinical management of cardiovascular risk factors in diabetes. The authors first review the unique challenges in adequately treating hypertension in this population, including obesity, and getting accurate blood pressure readings. The authors then discuss nonpharmacologic treatment options; and pharmacologic treatment, including with ACE inhibitors, ARBs (angiotensin receptor blockers), diuretics, beta blockers, calcium channel blockers, and combination therapy. The chapter concludes with a specific treatment plan and case presentation. 3 figures. 11 tables. 8 references.
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Hypertension: Management Strategies Source: in Mandal, A.K. and Nahman, N.S., Jr., eds. Kidney Disease in Primary Care. Baltimore, MD: Williams and Wilkins. 1998. p. 133-147. Contact: Available from Williams and Wilkins. 351 West Camden Street, Baltimore, MD 21201-2436. (800) 638-0672 or (410) 528-4223. Fax (800) 447-8438 or (410) 528-8550. E-mail:
[email protected]. PRICE: $39.95. ISBN: 0683300571. Summary: This chapter on hypertension (high blood pressure) is from a textbook that provides primary care physicians with practical approaches to common clinical problems of kidney diseases. The authors first provide background information about hypertension, including predisposing factors, the technique for blood pressure measurement, white coat hypertension, and pseudohypertension. The authors then discuss diagnostic considerations, including history, review of medications, physical examination, and laboratory evaluations; the causes of secondary hypertension; treatment, including nonpharmacologic approaches, medication selection based on populations, classes of antihypertensive medication, step therapy, and compliance issues; and how to manage refractory hypertension, including measuring sodium intake. The chapter concludes with a discussion of disability determination, the indications for referring a patient to a specialist, and the answers to a list of questions commonly asked by patients diagnosed with hypertension. The authors emphasize that patient compliance is essential to successful treatment of hypertension. 6 tables. 8 references.
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Nutritional Factors in Hypertension Source: in Kopple, J.D. and Massry, S.G. Nutritional Management of Renal Disease. Baltimore, MD: Williams and Wilkins. 1997. p. 77-95. Contact: Available from Williams and Wilkins. 351 West Camden Street, Baltimore, MD 21201-2436. (800) 638-0672 or (410) 528-4223. Fax (800) 447-8438 or (410) 528-8550. PRICE: $99.00. ISBN: 068304740X.
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Summary: This chapter on nutritional factors in hypertension is from a medical textbook on nutrition and metabolism of individuals with renal disease or renal failure. The pathophysiology of essential hypertension is complex and multifactorial. Both genetic and environmental factors concur in raising blood pressure in a substantial number of individuals. A variety of dietary and environmental factors, when combined with a predisposing genetic background, may lead to an elevation of blood pressure above normal. The authors focus on the role of several dietary factors in the pathophysiology of essential hypertension. They discuss the role of salt intake in hypertension, cardiovascular complications, and the risk of renal failure. Additional topics include potassium, chloride, calcium, magnesium, phosphorus, cadmium, meat protein, fiber, complex versus refined carbohydrates, dietary fats, fish oil, and alcohol intake. The authors describe why the role of dietary salt remains controversial. They also note that it is not uncommon to observe that patients with resistant hypertension abuse alcohol, and only a decrease in alcohol consumption improves the blood pressure control. 160 references. (AA-M). •
Portal Hypertension and Gastrointestinal Bleeding Source: in Friedman, L.S. and Keeffe, E.B., eds. Handbook of Liver Disease. Philadelphia, PA: Churchill-Livingstone. 1998. p. 139-149. Contact: Available from W.B. Saunders Company. Book Order Fulfillment Department, 6277 Sea Harbor Drive, Orlando, FL 32887-4430. (800) 545-2522. Fax (800) 874-6418. Email:
[email protected]. PRICE: $73.00 plus shipping and handling. ISBN: 0443055203. Summary: This chapter on portal hypertension and gastrointestinal bleeding is from a comprehensive handbook in outline format that offers easy access to information on the full range of liver disorders and covers symptoms, signs, differential diagnoses, and treatments. Patients with cirrhosis (liver scarring) who develop large esophageal varices (dilated veins) as a consequence of portal hypertension have a 25 to 35 percent risk of a variceal hemorrhage and a 30 to 50 percent mortality rate associated with the bleeding episode. Mortality depends on the clinical status of the patient and the severity of the bleeding episodes. Nonselective beta adrenergic blockers are the only proven therapy for preventing the first variceal hemorrhage in patients with cirrhosis. Both endoscopic therapy (sclerotherapy, variceal ligation) and drug therapy (vasopressin plus nitroglycerin, somatostatin, Glypressin) are effective in controlling the acute bleeding episode. The combination of endoscopic and pharmacologic therapy offers advantages over the use of either therapy alone. Endoscopic variceal ligation is the endoscopic treatment of choice for preventing recurrent variceal bleeding. Nonselective beta adrenergic blockers or combinations of beta blockers and long acting nitrates are effective in preventing recurrent variceal bleeding. Serial measurement of portal pressure is helpful in assessing the effectiveness of therapy and making appropriate changes when indicated. For patients failing medical therapy to prevent recurrent variceal hemorrhage, options include transjugular intrahepatic portosystemic stent shunts, surgical shunts, or liver transplantation. Selection of the appropriate rescue procedure is dictated by the clinical status of the patient, the availability of expertise in the procedure and, in the case of liver transplantation, appropriateness of the condition and availability of a donor organ. 2 tables. 9 references. (AA-M).
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Renovascular Hypertension Source: in Mandal, A.K. and Nahman, N.S., Jr., eds. Kidney Disease in Primary Care. Baltimore, MD: Williams and Wilkins. 1998. p. 148-157.
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Contact: Available from Williams and Wilkins. 351 West Camden Street, Baltimore, MD 21201-2436. (800) 638-0672 or (410) 528-4223. Fax (800) 447-8438 or (410) 528-8550. E-mail:
[email protected]. PRICE: $39.95. ISBN: 0683300571. Summary: This chapter on renovascular hypertension (a secondary form of high blood pressure resulting from renal artery stenosis, or RAS) is from a textbook that provides primary care physicians with practical approaches to common clinical problems of kidney diseases. The authors discuss the causes, including fibromuscular dysplasia and increased renal renin release; diagnostic considerations, including the patient history, physical examination, index of clinical suspicion, and confirmation of diagnosis; and treatment options, including renal artery angioplasty, surgical bypass procedures, and the medical management of documented renal artery stenosis. The chapter concludes with a discussion of the indications for referring a patient to a specialist and with the answers to a list of questions commonly asked by patients diagnosed with renovascular hypertension. The diagnosis of atherosclerotic RAS is usually considered in patients with difficult-to-control hypertension or in hypertensive patients with unexplained azotemia. The authors recommend renal artery angioplasty as firstline therapy in patients with atherosclerotic RAS. Medical management consists of good blood pressure control, preferably with antihypertensive drugs other than ACE inhibitors. ACE inhibitors should be avoided or used with great caution, as converting-enzyme drugs may further impair blood flow and worsen or precipitate azotemia. 2 figures. 4 tables. 6 references. •
Results of Hypertension Treatment Trials in Diabetic Patients Source: in Moser, M. and Sowers, J.R. Clinical Management of Cardiovascular Risk Factors in Diabetes. Caddo, OK: Professional Communications, Inc. 2002. p.71-117. Contact: Available from Professional Communications, Inc., Fulfillment Center, PO Box 10, Caddo, OK 74729-0010. (800)337-9838. Fax (580)367-9989. E-mail:
[email protected]. ISBN: 1884735665. PRICE: $21.95, plus shipping and handling. Summary: This chapter on the results of hypertension (high blood pressure) treatment trials in patients with diabetes is from a handbook that offers a concise overview of the clinical management of cardiovascular risk factors in diabetes. In recent years, definitive evidence has become available that lowering blood pressure will reduce morbidity (complications) and mortality (death) in patients with diabetes, probably to a greater extent even than controlling blood glucose levels. The evidence strongly suggests that in the young or old, male or female, treatment of elevated blood pressure and lowering it to goals below those set in nondiabetic patients will be beneficial. The authors review early clinical trials in patients with diabetes and hypertension; therapy for diabetic nephropathy (kidney disease associated with diabetes); the ABCD (Appropriate Blood Pressure Control in Diabetes) trial and the FACET (Fosinopril versus Amlodipine Cardiovascular Event Trial) research; the United Kingdom Prospective Diabetes Study (UKPDS); the Captopril Prevention Project Study; the Systolic Hypertension Trial in Europe (Syst-Eur); the HOT (Hypertension Optimal Treatment) trial; the role of angiotensin receptor blockers (ARBs) in the management of patients with diabetes; and the Heart Outcome Prevention Evaluation (HOPE) study. 11 figures. 14 tables. 18 references.
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Vascular Disorders of Kidney and Hypertension Source: in Blandy, J. Lecture Notes on Urology. Malden, MA: Blackwell Science, Inc. 1998. p.102-106. Contact: Available from Blackwell Science, Inc. 350 Main Street, Commerce Place, Malden, MA 02148. (800) 215-1000 or (617) 388-8250. Fax (617) 388-8270. E-mail:
[email protected]. Website: www.blackwell-science.com. PRICE: $39.95. ISBN: 0632042028. Summary: This chapter on vascular disorders of the kidney and hypertension (high blood pressure) is from an undergraduate medical textbook in the field of urology and urological surgery. The author discusses arterial infarction, venous thrombosis, aneurysm of the renal (kidney) artery, renal hypertension, and renal artery stenosis (narrowing). Much of the information is presented in diagrams or illustration format for ease of use. 7 figures. 5 references.
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What You Need to Know About Hypertension Source: in Hirsch, I.B. 12 Things You Must Know About Diabetes Care Right Now!. Alexandria, VA: American Diabetes Association. 2000. p. 101-114. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $14.95 plus shipping and handling. ISBN: 1580400612. Summary: This chapter provides information on hypertension. Although hypertension itself usually does not have symptoms as dramatic as those of eye or kidney disease, it is a serious problem that increases the risk of heart attack, eye problems, and kidney disease. Normal blood pressure is 120/80 mmHg. Hypertension results when blood pressure levels are consistently at 140/90 mmHg or above. Factors that influence whether a person will have hypertension include gender, race, age, how long a person has had diabetes, and whether protein is present in the urine. People who have type 2 diabetes are more likely to have hypertension than people who have type 1 diabetes. The United Kingdom Prospective Diabetes Study showed that improving hypertension control would reduce the risk of diabetes related complications. The diagnosis of hypertension should be based on blood pressure measurements obtained on at least three different occasions. The American Diabetes Association recommends that the goal of blood pressure therapy for people older than 18 who have diabetes is to keep blood pressure below 130/85 mmHg. Mild to moderate hypertension may be treated with lifestyle changes before beginning drug therapy. These changes include losing weight, restricting sodium, quitting smoking, limiting daily alcohol intake to less than 2 ounces, and doing regular aerobic exercise. Drugs available to treat hypertension include thiazide diuretics, beta blockers, angiotensin converting enzyme inhibitors, calcium channel blockers, and alpha blockers. The chapter discusses the effects of these drugs and highlights factors that people need to consider about these drugs. In addition, the chapter includes a list of questions a patient may ask a doctor and questions a doctor may ask a patient. 3 tables.
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Insulin Resistance and Hypertension Source: in Schrier, R.W. and Wilcox, C.S., eds. Atlas of Diseases of the Kidney. Volume 3: Hypertension and the Kidney. Philadelphia, PA: Current Medicine, Inc. 1999. p. 5.1-5.10.
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Contact: Available from Blackwell Science, Inc. 350 Main Street, Malden, MA 02148. (800) 215-1000 or (781) 388-8250. Fax (781) 388-8270. E-mail:
[email protected]. PRICE: $75.00 plus shipping and handling. ISBN: 063204389X. Summary: This chapter uses a series of figures to discuss insulin resistance and hypertension. Insulin resistance is associated with increased risk of cardiovascular disease, and it may be the link between hypertension and dyslipidemia. Data show that approximately 25 percent to 40 percent of nonobese, nondiabetic patients who have hypertension are insulin resistant. Researchers have also observed insulin resistance in genetic and acquired animal models of hypertension. A syndrome, termed syndrome X, includes a constellation of insulin resistance, decreased high density lipoprotein cholesterol, and hypertension. Although various causes have been proposed, it is unclear whether insulin resistance or reactive hyperinsulinemia, or both, actually cause hypertension. Recent findings that insulin sensitizing agents attenuate the development of hypertension provide support for this hypothesis. However, these agents may lower blood pressure by different mechanisms. Type 2 diabetes represents an extreme of insulin resistance. The prevalence of hypertension increases twofold to threefold among people who have diabetes. Hypertension is associated with a fourfold increase in mortality among patients who have type 2 diabetes, and antihypertensive drug therapy has a beneficial effect on both macrovascular and microvascular disease. Although there is some concern that diuretics may augment insulin resistance, people who have diabetes benefit from antihypertensive therapy with diuretics. Different antihypertensive drugs have different renal protective effects. Angiotensin converting enzyme inhibitors decrease proteinuria and retard the progression of renal insufficiency in people who have diabetes but normal blood pressure and hypertension. Findings from studies evaluating the effects of calcium antagonists on the progression of diabetic nephropathy are varied. Additional studies are needed to evaluate the antihypertensive potential of insulin sensitizing agents in people who have type 2 diabetes. 31 figures. 19 references. •
Counseling Patients with Hypertension and Diabetes Mellitus Source: in Mandal, A.K. and Nahman, N.S., Jr., eds. Kidney Disease in Primary Care. Baltimore, MD: Williams and Wilkins. 1998. p. 266-270. Contact: Available from Williams and Wilkins. 351 West Camden Street, Baltimore, MD 21201-2436. (800) 638-0672 or (410) 528-4223. Fax (800) 447-8438 or (410) 528-8550. E-mail:
[email protected]. PRICE: $39.95. ISBN: 0683300571. Summary: This chapter, from a book about kidney disease in primary care, provides information about counseling people with hypertension and diabetes. The author points out that people with both hypertension and diabetes have an increased incidence of renal disease, which accompanies other risk factors such as dyslipidemia, increased fibrinogen, hyperuricemia, and left ventricular hypertrophy. Hypertension adds to the morbidity and mortality of diabetes. Both hypertension and diabetes should be diagnosed early and treated aggressively through medication, counseling, and education. Topics include medications in coexisting conditions, overcoming barriers and identifying patient needs, developing a teaching or counseling plan, evaluating learning outcomes, and choosing and evaluating counseling tools and techniques. The chapter stresses the importance of the health care professional's positive attitude in counseling the patient. In addition, when regimens are simple, understandable, and reinforced, compliance with long term therapy is improved. Key points and a list of nine suggested readings conclude the chapter. (AA-M).
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Hypertension in Persons with Diabetes Source: in Powers, M.A., ed. Handbook of Diabetes Medical Nutrition Therapy. Gaithersburg, MD: Aspen Publishers, Inc. 1996. p. 571-584. Contact: Available from Aspen Publishers. P.O. Box 990, Frederick, MD 21705-9727. (800) 638-8437. Fax (301) 695-7931. PRICE: $89.00. ISBN: 0834206315. Summary: This chapter, from a handbook on diabetes medical nutrition therapy (MNT), discusses hypertension in persons with diabetes. The authors note that hypertension is associated with increased risk of diabetic complications, and the risk factors for developing diabetes and hypertension overlap considerably. Topics include the epidemiology and natural history of hypertension and diabetes; blood pressure measurement; risk factors; the classification of hypertension; treatment modalities including antihypertensive medications, weight reduction, sodium restriction, and other dietary and lifestyle modifications; and individualizing nutrition therapy. 5 figures. 35 references.
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Hypertension and Diabetic Vascular Complications Source: in Schrier, R.W., et al., eds. Advances in Internal Medicine. Vol 39. St. Louis, MO: Mosby-Year Book, Inc. 1994. p. 633-665. Contact: Available from Mosby Year-Book, Inc. 11830 Westline Industrial Drive, St. Louis, MO 63146. (800) 426-4545. Fax (800) 535-9935. E-mail:
[email protected]. PRICE: $72.95. ISBN: 0815183127. ISSN: 00652822. Summary: This chapter, from a text on advances in internal medicine, reviews hypertension and the vascular complications of diabetes. The authors note that the major vascular complications of diabetes fall into two basic categories: microvascular (retinopathy and nephropathy) and macrovascular (cardiovascular, cerebrovascular, and peripheral vascular) disease. The incidence of hypertension is increased in the population with diabetes, compared to the nondiabetic population. Topics include the effects of diabetes and hypertension on vascular biology; endothelial dysfunction in diabetes and in hypertension; the effects of endothelial cell damage on smooth muscle; risk factors that contribute to the development of atherosclerosis in diabetes; diabetic nephropathy; diabetic retinopathy; the prevention and early recognition of the microvascular complications of diabetes; managing hyperglycemia, hypertension, and hyperlipidemia; prognostic indicators; control of oxidation; platelet abnormalities; and gene therapy. 5 tables. 197 references.
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Arterial Hypertension: Lessons from Patient Education Source: in Assal, J., Golay, A., and Visser, A.P., eds. New Trends in Patient Education: A Trans-Cultural and Inter-Disease Approach. Amsterdam, The Netherlands: Elsevier Science B.V. 1995. p. 37-55. Contact: Available from Elsevier Science. Regional Sales Office, Customer Support Department, 655 Avenue of the Americas, New York, NY 10010. (212) 633-3730. Fax (212) 633-3680. E-mail:
[email protected]. PRICE: $209.50. ISBN: 0444822348. Summary: This chapter, from the proceedings of an international patient education conference, discusses arterial hypertension and patient education. The author asserts that patient education has been instrumental in bringing about tremendous improvements in hypertension-related mortality, morbidity, life expectancy, and life quality. Patient education has evolved from an adjunct to medical therapy to an
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intervention in its own right. In this process, patient education tasks and techniques themselves have undergone remarkable developments, driven by evolving patient needs due to medical progress. The same is true for the roles of patients and health care providers. Dealing with hypertension is a behavior change process which demands serious learning efforts from all parties involved: patients, health care providers, and health care administrators. The author emphasizes processes and tools for effective patient education, including preventive behavior change and risk factor management. 7 figures. 12 tables. 57 references. (AA-M). •
Diabetes and Hypertension Source: in Johnstone, M.T. and Veves, A. Diabetes and Cardiovascular Disease. Totowa, NJ: The Humana Press, Inc. 2001. p. 123-129. Contact: Humana Press, Inc. 999 Riverview Dr., Suite 208 Totowa, NJ 07512. (973) 2561699. Fax (973) 256-8341. E-mail:
[email protected] PRICE: $125.00, plus shipping and handling. ISBN: 089603755X. Summary: With over ten million diagnosed patients and another five million undiagnosed, diabetes mellitus and its complications is a major public health problem that will assume epidemic proportions as the population grows older. This chapter on diabetes and hypertension is from a textbook that offers physicians practical knowledge about cardiovascular disease and diabetes. This chapter is in Part I, which focuses on pathophysiology, including the mechanisms and risk factors for diabetic cardiovascular disease. The author notes that many factors contribute to increased cardiovascular disease (CVD) in persons with diabetes. These factors include hypertension (high blood pressure), dyslipidemia (disordered levels of fats in the blood), platelet hyperactivity, endothelial (the cells lining the body cavity and cardiovascular system) abnormalities, as well as hyperglycemia (high blood glucose), microalbuminuria (protein in the urine), and hyperinsulinemia (high levels of insulin in the blood). The author discusses characteristics of hypertension in people with diabetes and then focuses on treatment goals in this population. The goal of hypertension treatment in persons with diabetes is to prevent hypertension-associated death and disability. The level of blood pressure and the diagnosis of hypertension should be based on multiple blood pressure measurements obtained in a standardized fashion on at least three occasions. Because of the tendency to orthostatic hypotension (abnormally low blood pressure upon standing), standing blood pressures should be measured at each office visit. Pharmacologic (drug) therapy should be initiated when lifestyle modifications do not lower blood pressure to less than 130 over 85 mmHg in people with diabetes. Combination therapy is usually necessary for adequate blood pressure control; therapy should include an ACE inhibitor for maximal benefits in protecting against cardiovascular disease as well as renal (kidney) disease. 1 figure. 1 table. 30 references.
Directories In addition to the references and resources discussed earlier in this chapter, a number of directories relating to hypertension have been published that consolidate information across various sources. The Combined Health Information Database lists the following, which you may wish to consult in your local medical library:12 12
You will need to limit your search to “Directory” and “hypertension” using the "Detailed Search" option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find directories, use the drop boxes at
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Asian Language: Sources of Health Materials Source: Washington, DC: Office of Minority Health Resource Center. 199x. [11 p.]. Contact: Available from Office of Minority Health Resource Center. P.O. Box 37337, Washington, DC 20013-7337. (800) 444-6472. Website: www.omhrc.gov. PRICE: Single copy free. Summary: This directory lists sources identified by the Office of Minority Health Resource Center (OMH RC) that produce or distribute health promotion materials in various Asian languages. Materials concentrate on minority health priority areas and associated risk factors: cancer, cardiovascular diseases and stroke, chemical dependency, diabetes, infant mortality, homicide, suicide, and unintentional injury. Sources of AIDS information and educational materials are also included. Topics related to kidney and urologic diseases include AIDS, cultural awareness, high blood pressure (hypertension), lupus, men's health, nutrition, sexually transmitted diseases, and women's health. Sources are arranged alphabetically. Organization entries include organization name, address, telephone number, source title, and annotation. The primary languages in which the organization provides materials are noted. Organizations should be contacted directly to determine the cost and availability of bulk quantities or for permission to photocopy.
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Complete Directory for People with Chronic Illness. 4th ed Source: Lakeville, CT: Grey House Publishing, Inc. 2000. 1009 p. Contact: Available from Grey House Publishing, Inc. Pocket Knife Square, Lakeville, CT 06039. (860) 435-0868. Fax (860) 435-0867. PRICE: $165.00. ISBN: 0939300931. Summary: This directory provides a comprehensive overview of the support services and information resources available for people with any of 80 specific chronic illnesses. It presents information on various organizations, educational materials, publications, and databases. A chapter is devoted to each chronic illness and includes a brief description of it. The sections related to kidney and urologic diseases include: AIDS, Alzheimer's disease, cancer, cerebral palsy, diabetes, hypertension, impotence, incontinence, infertility, kidney disease, multiple sclerosis, sexually transmitted diseases, spina bifida, stroke, and substance abuse. The description of each disease is followed by subchapters that identify national and State associations and agencies, libraries, research centers, reference books, children's books, magazines, newsletters, pamphlets, videotapes and films, support groups and hotlines, and websites. In addition, the directory includes a chapter on death and bereavement, as well as a chapter on Wish Foundations for terminally and chronically ill children.
the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Select your preferred language and the format option “Directory.” Type “hypertension” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months.
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CHAPTER 8. MULTIMEDIA ON HYPERTENSION Overview In this chapter, we show you how to keep current on multimedia sources of information on hypertension. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.
Video Recordings An excellent source of multimedia information on hypertension is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “hypertension” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “hypertension” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on hypertension: •
Hypertension and Nutrition Source: Los Angeles, CA: National Health Video, 15 min., 1995. Contact: National Health Video. 12021 Wilshire Blvd., Suite 550, Los Angeles, CA 90025. 1-800-543-6803. Summary: This video explains the role of diet in managing hypertension. It also demonstrates recipes. The video is accompanied by an instruction resource package that includes learning objectives and activities, a before-after knowledge quiz, and handout masters.
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Pediatric Hypertension Source: New Hyde Park, NY: Schneider Children's Hospital. 2000. (Videorecording).
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Contact: Available from Schneider Children's Hospital. 269-01 76th Avenue, Room 365, New Hyde Park, New York 11040-1432. (718) 470-3491. Fax: (718) 470-0887. Website: www.schneiderchildrenshospital.org. Summary: This videotape program educates parents and families of children who are diagnosed with hypertension (high blood pressure). The program is narrated by three health care providers: Dr. Julie Ingelfinger, Dr. Howard Trachtman, and Rachel Frank, a nephrology nurse. The program explains why it is vital to diagnose and manage pediatric hypertension, noting the role of long term hypertension in adult problems of heart attack, stroke, and congestive heart failure. The program reviews hypertension and its causes, treatment options, how to understand blood pressure readings (systolic and diastolic), classification of the different levels of hypertension, risk factors, diagnostic considerations and tests, and management options, including nutrition, drug therapy, weight control, exercise, relaxation methods, and refraining from smoking. The program features many interviews with children and parents and their health care providers.
Audio Recordings The Combined Health Information Database contains abstracts on audio productions. To search CHID, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find audio productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Sound Recordings.” Type “hypertension” (or synonyms) into the “For these words:” box. The following is a typical result when searching for sound recordings on hypertension: •
Nutrition in the Pathogenesis and Treatment of Hypertension Source: Bethlehem, PA: St. Luke's Hospital. 1991. Contact: Available from St. Luke's Hospital. Nutrition Services-Renal, 801 Ostrum Street, Bethlehem, PA 18015. (215)954-4000. PRICE: Contact directly for details. Summary: This audiocassette presents a program from a one-day symposium, held in October 1991, that focuses on the nutritional assessment and nutritional intervention in the treatment of patients with chronic renal failure (CRF). The speaker, G. Gopal Krishna, an associate professor of medicine, discusses nutrition in the pathogenesis and treatment of hypertension. The symposium was designed for dietitians and for students studying to become dietitians.
Bibliography: Multimedia on Hypertension The National Library of Medicine is a rich source of information on healthcare-related multimedia productions including slides, computer software, and databases. To access the multimedia database, go to the following Web site: http://locatorplus.gov/. Select “Search LOCATORplus.” Once in the search area, simply type in hypertension (or synonyms). Then, in the option box provided below the search box, select “Audiovisuals and Computer Files.” From there, you can choose to sort results by publication date, author, or relevance. The following multimedia has been indexed on hypertension: •
A Rational approach to newly discovered hypertension [slide] Source: University of Michigan, Medical Center, Department of Postgraduate Medicine and Health
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Professions Education, Independent Study Unit; Year: 1974; Format: Slide; Ann Arbor: The University: [for loan or sale by its Medical Center, Media Library], c1974 •
Assessment of the client with hypertension [sound recording] Source: Niagara University, College of Medicine; Year: 1977; Format: Sound recording; Buffalo: Communications in Learning, 1977
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Clinical management of hypertension [videorecording] Source: Edward D. Freis; Year: 1976; Format: Videorecording; New York: Medcom, c1976
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Clinical pharmacology - antihypertensive agents [sound recording] Source: American College of Physicians; produced by Audio-Digest Foundation; Year: 1976; Format: Sound recording; Glendale, Calif.: The Foundation, p1976
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Evaluation of the hypertensive patient [videorecording] Source: Emory University School of Medicine; Year: 1974; Format: Videorecording; Atlanta: Georgia Regional Medical Television Network: [for loan or sale by A. W. Calhoun Medical Library, 1974]
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Hypertension: the challenge of diagnosis [motion picture] Source: American Heart Association; [made by] Harvest Films; Year: 1968; Format: Motion picture; [New York]: The Association, c1968
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Hypertension: your patient and you [filmstrip] Source: Trainex Corporation; Year: 1974; Format: Filmstrip; [Garden Grove, Calif.]: Trainex, c1973
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Hypertension [slide] Source: Department of Continuing Medical Education School of Medicine State University of New York at Buffalo, in cooperation with the Lakes Area Regional Medical Program; Year: 1975; Format: Slide; [Buffalo]: Communications in Learning, 1975
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Hypertension [videorecording] Source: Emory University School of Medicine; Year: 1974; Format: Videorecording; Atlanta: Georgia Regional Medical Television Network, [1974]
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Hypertension [videorecording]: management in perspective. Year: 1982; Format: Videorecording; New York: Network for Continuing Medical Education, 1982
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Hypertension and the brain [videorecording] Source: Emory University School of Medicine; Year: 1974; Format: Videorecording; Atlanta: Georgia Regional Medical Television Network: [for loan or sale by A. W. Calhoun Medical Library, 1974]
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Hypertension and the vascular tree (in the kidney) [videorecording] Source: Emory University School of Medicine; Year: 1974; Format: Videorecording; Atlanta: Georgia Regional Medical Television Network: [for loan or sale by A. W. Calhoun Medical Library, 1974]
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Hypertension update [videorecording]. Year: 2003; Format: Videorecording; Secaucus, NJ: Network for Continuing Medical Education, c2003
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Hypertensive crisis [videorecording] Source: Dept. of Continuing Education, Harvard Medical School and the Massachusetts General Hospital, Emergency Training Course; produced by Health Educations Programs, Inc; Year: 1973; Format: Videorecording; [Minneapolis]: Institute for Continuing Physician Education, c1973
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Interposition mesocaval shunt for portal hypertension [motion picture] Source: Theodore Drapanas; produced by Davis & Geck; Year: 1972; Format: Motion picture; Danbury, Conn.: Davis & Geck, 1972
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Is hypertension essential [videorecording] Source: Emory University School of Medicine; Year: 1975; Format: Videorecording; Atlanta: Georgia Regional Medical Television Network: [for loan or sale by A. W. Calhoun Medical Library, 1975]
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Modern pharmacological management of systemic hypertension [slide] Source: American Heart Association; Year: 1971; Format: Slide; [New York: The Association, 1971]
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Portal hypertension & ascites [slide] Source: American Gastroenterological; Year: 1976; Format: Slide; [Thorofare, N. J.]: The Association; [Baltimore, Md.: for sale by MilnerFenwick], c1975
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Renal vascular hypertension [motion picture]: an approach to diagnosis and treatment Source: the University of Texas Medical Branch; Year: 1965; Format: Motion picture; United States: The University, [1965]
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Roentgenologic assessment of renal hypertension [slide] Source: Radiological Society of North America; Year: 1975; Format: Slide; [Chicago]: The Society: [for loan or sale by its Educational Materials Division], c1975
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Side-to-side portacaval anastomosis for portal hypertension [motion picture] Source: produced and distributed by American Cyanamid Company, Surgical Products Division; Year: 1968; Format: Motion picture; United States: Davis & Geck, [1968]
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Surgical treatment of portal hypertension [motion picture] Source: Richard C. Britton; [made by] Department of Medical Illustration, Cleveland Clinic; Year: 1963; Format: Motion picture; Cleveland: The Clinic; [Atlanta: for loan by National Medical Audiovisual Center, 1963?]
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The Distal splenorenal shunt in the therapy of bleeding esophageal varices due to portal hypertension [motion picture]: demonstrating selective decompression of esophagogastric varices Source: Robert Zeppa, Duane G. Hutson; produced by Davis& Geck; Year: 1972; Format: Motion picture; Danbury, Conn.: Davis & Geck, [1972]
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The Initial office evaluation of the patient with hypertension [videorecording] Source: Emory University School of Medicine; Year: 1977; Format: Videorecording; Atlanta: Georgia Regional Medical Television Network: [for loan or sale by A. W. Calhoun Medical Library, 1977]
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CHAPTER 9. PERIODICALS AND NEWS ON HYPERTENSION Overview In this chapter, we suggest a number of news sources and present various periodicals that cover hypertension.
News Services and Press Releases One of the simplest ways of tracking press releases on hypertension is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing. PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “hypertension” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance. Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to hypertension. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “hypertension” (or synonyms). The following was recently listed in this archive for hypertension:
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Nisoldipine ER as effective as amlodipine in blacks with hypertension Source: Reuters Industry Breifing Date: October 16, 2003
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Hsp70 levels have prognostic value in hypertensive patients Source: Reuters Industry Breifing Date: October 03, 2003
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COX-2 inhibitor reverses endothelial dysfunction in hypertensive patients Source: Reuters Industry Breifing Date: October 01, 2003
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Timing of valsartan dosing has no effect on antihypertensive effects Source: Reuters Industry Breifing Date: September 25, 2003
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Low adiponectin linked to risk for hypertension Source: Reuters Medical News Date: September 24, 2003
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Diabetes is main determinant of silent cerebral infarcts in hypertensive patients Source: Reuters Medical News Date: September 18, 2003
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HHV-8 may play role in primary pulmonary hypertension Source: Reuters Medical News Date: September 17, 2003
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Diuretic recommended over alpha-blocker as first-line antihypertensive therapy Source: Reuters Industry Breifing Date: September 10, 2003
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Trial data show Tracleer effective for HIV-related pulmonary hypertension Source: Reuters Medical News Date: September 02, 2003
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ECG index improves cardiovascular risk stratification in essential hypertension Source: Reuters Medical News Date: September 01, 2003
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Positional change in blood pressure related to subsequent hypertension Source: Reuters Medical News Date: August 29, 2003
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Urban sprawl increases risk of obesity, hypertension Source: Reuters Medical News Date: August 28, 2003
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Sustained release indapamide helpful in diabetic hypertensives Source: Reuters Industry Breifing Date: August 28, 2003
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Weight loss reduces left ventricular mass in untreated hypertensives Source: Reuters Industry Breifing Date: August 27, 2003
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Modest exercise reduces blood pressure in sedentary hypertensives Source: Reuters Medical News Date: August 13, 2003
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Hypertension continues to damage organ systems in elderly Source: Reuters Medical News Date: August 05, 2003
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Genetic factors influence course of salt-sensitive hypertension Source: Reuters Medical News Date: July 23, 2003
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Nephrectomy benefits some patients with renovascular hypertension Source: Reuters Medical News Date: July 17, 2003
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Alteon hypertension drug fails to meet main goal Source: Reuters Health eLine Date: July 17, 2003
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Alteon hypertension drug fails to achieve main goal. Source: Reuters Industry Breifing Date: July 17, 2003
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Baroreflex suppression of sympathetic activity tied to obesity hypertension Source: Reuters Medical News Date: July 16, 2003
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RAS blockade improves insulin sensitivity in essential hypertension Source: Reuters Industry Breifing Date: July 15, 2003
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U.S. rate of hypertension rises in 1990s - study Source: Reuters Health eLine Date: July 08, 2003
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Hypertension on the rise in the US Source: Reuters Medical News Date: July 08, 2003
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Level of C-reactive protein may be a risk factor for hypertension Source: Reuters Medical News Date: July 03, 2003
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Slow breathing improves drug-resistant hypertension Source: Reuters Industry Breifing Date: July 02, 2003
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Sildenafil shows promise as adjunct therapy for severe pulmonary hypertension Source: Reuters Industry Breifing Date: July 02, 2003
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Arginine promising as treatment for pulmonary hypertension in sickle cell patients Source: Reuters Industry Breifing Date: July 01, 2003
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Nonselective screening of hypertensives yields high-rate of primary aldosteronism Source: Reuters Medical News Date: June 19, 2003
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The NIH Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “hypertension” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “hypertension” (or synonyms). If you know the name of a company that is relevant to hypertension, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/. BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “hypertension” (or synonyms).
Newsletters on Hypertension Find newsletters on hypertension using the Combined Health Information Database (CHID). You will need to use the “Detailed Search” option. To access CHID, go to the
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following hyperlink: http://chid.nih.gov/detail/detail.html. Limit your search to “Newsletter” and “hypertension.” Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter.” Type “hypertension” (or synonyms) into the “For these words:” box. The following list was generated using the options described above: •
Kidney Disease Source: Sarcoidosis Networking. 8(3): 2. May-June 2000. Contact: Available from Sarcoid Network Association. Sarcoidosis Networking, 13925 80th Street East, Puyallup, WA 98372-3614. Email:
[email protected]. Summary: Sarcoidosis is a chronic, progressive systemic granulomatous (causing lesions) disease of unknown cause (etiology), involving almost any organ or tissue, including the skin, lungs, lymph nodes, liver, spleen, eyes, and small bones of the hands or feet. This brief article, from a newsletter for patients with sarcoidosis, reviews kidney disease, its types, diagnosis, and management. The article begins with a summary of the anatomy and function of the kidneys, which filter the blood (removing waste and excess body fluids), and maintain the balance of some essential nutrients helping to regulate blood pressure, red blood cells, and elements such as potassium and calcium. Without functioning kidneys, one cannot live without dialysis, the mechanical filtration of the blood. Kidneys fail for a variety of reasons, including trauma to the kidney, toxins, heart failure, obstruction (kidney stones), overuse of some medications, and diseases that invade the kidney, such as sarcoidosis. Diabetes and high blood pressure are the most common causes for loss of kidney function. Warning signs of kidney disease are high blood pressure (hypertension), blood or protein in the urine, creatinine level greater than 1.2 in women or 1.4 in men, more frequent urination (especially at night), difficult or painful urination, and puffy eyes or swelling of the hands or feet (especially in children). Loss of kidney function can produce symptoms including fatigue, weakness, nausea, vomiting, diarrhea or constipation, headaches, loss of appetite, increased edema (fluid retention), and fever or chills. Kidney failure is characterized as acute kidney failure, chronic kidney insufficiency, and chronic kidney failure. The need to put a person on dialysis depends upon the levels of creatinine and urea nitrogen in the blood and the evaluation of body parameters such as fluid status, and symptoms of toxicity. The author encourages readers to practice preventive measures which include drinking 8 to 10 glasses of water per day, preventing or treating diabetes and high blood pressure, avoiding tobacco, eating a well balanced diet, practicing good hygiene, treating wounds and infections, limiting exposure to heavy metals and toxic chemicals, and avoiding unnecessary over the counter drug use.
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AGS Newsletter. [Newsletter] Source: New York, NY: American Geriatrics Society. [12 p. average]. Contact: Available from American Geriatrics Society. 770 Lexington Avenue, Suite 300, New York, NY 10021. (212) 308-1414. PRICE: Free. Summary: This newsletter, published bimonthly by the American Geriatrics Society, contains articles and updates about issues affecting the elderly, including Alzheimer's disease and dementia. A typical newsletter includes a letter from the president of the American Geriatrics Society, four to five articles, updates about treatment and caregiving, and meeting highlights. In a sample issue, May-June 1992, the lead article reported on an incontinence education campaign launched by the National Institute on Aging and the Alliance for Aging Research and targeted to professionals and the public.
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The other four articles discuss nondrug therapies for hypertension, funding for adult day care programs, restraint use, and long term care nursing shortages. The newsletter also includes updates about available research grants, recognition of medical professionals for their work in long term care, a listing of job opportunities at health care facilities around the country, new publications, and notices of upcoming courses and conferences.
Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “hypertension” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on hypertension: •
Hypertension in Caregivers, Part II: Controlling Your Own Stress Level Source: Advocate. Alzheimer's Association of Greater Washington, DC Chapter. [Newsletter] p. 2-3. October 1990. Contact: Available from Alzheimer's Association of Greater Washington, DC Chapter. 7910 Woodmont Avenue, Suite 1100, Bethesda, MD 20814. (301) 652-6446. PRICE: Single copy free. Summary: This article suggests ways in which caregivers of Alzheimer's disease patients can control the stress caused by the demands placed upon them. The technique known as the Relaxation Response is outlined.
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Hypertension Drugs: They Can Treat More Than High Blood Pressure Source: Mayo Clinic Health Letter. 17(11): 5. November 1999. Contact: Available from Mayo Clinic Health Letter. Subscription Services, P.O. Box 53889, Boulder, CO 80322-3889. (800) 333-9037 or (303) 604-1465. Summary: This health newsletter article reviews the drugs used to treat hypertension (high blood pressure). The author focuses on the additional benefits of these drugs. Not only do hypertension drugs help control elevated blood pressure, but some actually offer additional health benefits. These can include treating heart failure, diabetes, or symptoms resulting from an enlarged prostate. There are several types of hypertension drugs, and each type helps control elevated blood pressure in a different way. These include diuretics, beta blockers, angiotensin converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, calcium channel blockers, alpha blockers, and central acting agents (central adrenergic inhibitors). In choosing drug therapy to treat a specific patient's hypertension, the physician will consider age, overall health, other medications already being taken, and cost considerations. One table outlines the possible additional health benefits these drugs have beyond treating elevated blood pressure. 1 table.
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Pulmonary Arterial Hypertension in Scleroderma: A New Treatment Source: Scleroderma Voice. Number 2: 9-10,23. 2002.
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Contact: Available from Scleroderma Foundation. 12 Kent Way, Suite 101, Byfield, MA 01922. (800) 722-HOPE or (978) 463-5843. Fax (978) 463-5809. E-mail:
[email protected]. Website: www.scleroderma.org. Summary: This newsletter article provides health professionals and people who have scleroderma with information on the diagnosis and treatment of pulmonary arterial hypertension (PAH). This serious condition occurs when the blood vessels that supply the lungs constrict, making it more difficult for blood to get through to the lungs. As time passes, scarring makes the vessels stiffer and thicker. The extra stress on the heart causes it to enlarge and become less flexible. As a result, less and less blood flows out of the heart, through the lungs, and into the body. PAH can occur by itself or in association with another disease. Scleroderma is the most common disease associated with PAH. It is more common in patients with limited scleroderma. The exact cause of PAH is unknown. However, many factors may have a role in the process of blood vessel thickening and stiffening, including the elevation of a substance in the body called endothelin, a potent vasoconstrictor. Symptoms of PAH include shortness of breath during exercise and at rest, chest pain, dizziness, and fainting. Diagnosis of PAH related to scleroderma is based on the results of a series of tests given to determine the specific cause of shortness of breath, including pulmonary function tests, chest x rays, high resolution computed tomography scans, scans for blood clots, and bronchoscopy. Doppler echocardiogram is the best screening tool for PAH. A right heart catheterization can confirm a diagnosis. Medications that relax and open up blood vessels are the mainstay of treatment for PAH; they include calcium channel blockers such as nifedifine or diltiazem, water pills, blood thinners, and drugs that block endothelin such as bosentan. Bosentan is the first oral medication approved by the Food and Drug Administration to block endothelin receptors. The drug is generally well tolerated, and it may have additional treatment applications in patients with scleroderma. 5 references.
Academic Periodicals covering Hypertension Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to hypertension. In addition to these sources, you can search for articles covering hypertension that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 10. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for hypertension. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with hypertension. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The
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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to hypertension: Amlodipine •
Systemic - U.S. Brands: Norvasc http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202670.html
Amlodipine and Benazepril •
Systemic - U.S. Brands: Lotrel http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203634.html
Angiotensin-Converting Enzyme (Ace) Inhibitors •
Systemic - U.S. Brands: Accupril; Aceon; Altace; Capoten; Lotensin; Mavik; Monopril; Prinivil; Univasc; Vasotec 4; Zestril http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202044.html
Angiotensin-Converting Enzyme (Ace) Inhibitors and Hydrochlorothiazide •
Systemic - U.S. Brands: Accuretic; Capozide; Lotensin HCT; Prinzide; Uniretic; Vaseretic; Zestoretic http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202045.html
Apraclonidine •
Ophthalmic - U.S. Brands: Iopidine http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202070.html
Beta-Adrenergic Blocking Agents •
Systemic - U.S. Brands: Betapace; Blocadren; Cartrol; Corgard; Inderal; Inderal LA; Kerlone; Levatol; Lopressor; Normodyne; Sectral; Tenormin; Toprol-XL; Trandate; Visken; Zebeta http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202087.html
Beta-Adrenergic Blocking Agents and Thiazide Diuretics •
Systemic - U.S. Brands: Corzide 40/5; Corzide 80/5; Inderide; Inderide LA; Lopressor HCT; Tenoretic 100; Tenoretic 50; Timolide 10-25; Ziac http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202088.html
Brimonidine •
Ophthalmic - U.S. Brands: Alphagan http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203130.html
Brinzolamide •
Ophthalmic - U.S. Brands: Azopt http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203544.html
Calcium Channel Blocking Agents •
Systemic - U.S. Brands: Adalat; Adalat CC; Calan; Calan SR; Cardene; Cardizem; Cardizem CD; Cardizem SR; Dilacor-XR; DynaCirc; Isoptin; Isoptin SR; Nimotop; Plendil; Procardia; Procardia XL; Vascor; Verelan http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202107.html
Researching Medications 391
Candesartan •
Systemic - U.S. Brands: Atacand http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203598.html
Carbachol •
Ophthalmic - U.S. Brands: Carbastat; Carboptic; Miostat http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202110.html
Carvedilol •
Systemic - U.S. Brands: Coreg http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203636.html
Clonidine •
Systemic - U.S. Brands: Catapres; Catapres-TTS http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202152.html
Clonidine and Chlorthalidone •
Systemic - U.S. Brands: Combipres http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202153.html
Diazoxide •
Oral - U.S. Brands: Proglycem http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202191.html
Diuretics, Loop •
Systemic - U.S. Brands: Bumex; Edecrin; Lasix; Myrosemide http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202205.html
Diuretics, Potassium-Sparing •
Systemic - U.S. Brands: Aldactone; Dyrenium; Midamor http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202206.html
Diuretics, Potassium-Sparing, and Hydrochlorothiazide •
Systemic - U.S. Brands: Aldactazide; Dyazide; Maxzide; Moduretic; Spirozide http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202207.html
Diuretics, Thiazide •
Systemic - U.S. Brands: Aquatensen; Diucardin; Diulo; Diuril; Enduron; Esidrix; Hydro-chlor; Hydro-D; HydroDIURIL; Hydromox; Hygroton; Metahydrin; Microzide; Mykrox; Naqua; Naturetin; Oretic; Renese; Saluron; Thalitone; Trichlorex 10; Zaroxolyn http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202208.html
Dorzolamide •
Ophthalmic - U.S. Brands: Trusopt http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202773.html
392 Hypertension
Dorzolamide and Timolol •
Ophthalmic - U.S. Brands: Cosopt http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203550.html
Doxazosin •
Systemic - U.S. Brands: Cardura http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202629.html
Enalapril and Felodipine •
Systemic - U.S. Brands: Lexxel http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203638.html
Epoprostenol •
Systemic - U.S. Brands: Flolan http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203429.html
Eprosartan •
Systemic - U.S. Brands: Teveten http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500044.html
Guanabenz •
Systemic - U.S. Brands: Wytensin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202271.html
Guanadrel •
Systemic - U.S. Brands: Hylorel http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202272.html
Guanethidine •
Systemic - U.S. Brands: Ismelin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202273.html
Guanfacine •
Systemic - U.S. Brands: Tenex http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202275.html
Hydralazine •
Systemic - U.S. Brands: http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202273.html
Hydralazine and Hydrochlorothiazide •
Systemic - U.S. Brands: Apresazide http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202286.html
Indapamide •
Systemic - U.S. Brands: Lozol http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202296.html
Researching Medications 393
Insulin •
Systemic - U.S. Brands: Humulin 50/50; Humulin 70/30; Humulin 70/30 Pen; Humulin L; Humulin N; Humulin N Pen; Humulin R; Humulin R, Regular U500 (Concentrated); Humulin U; Lente; Lente Iletin II; Novolin 70/30; Novolin 70/30 PenFill; Novolin 70/30 Prefilled; Novolin L; Novoli http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203298.html
Irbesartan •
Systemic - U.S. Brands: Avapro http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203379.html
Latanoprost •
Ophthalmic - U.S. Brands: Xalatan http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203607.html
Laxatives •
Oral - U.S. Brands: Afko-Lube; Afko-Lube Lax 40; Agoral Marshmallow; Agoral Raspberry; Alaxin; Alophen; Alphamul; Alramucil Orange; Alramucil Regular; Bilagog; Bilax; Bisac-Evac; Black-Draught; Black-Draught Lax-Senna; Carter's Little Pills; Cholac; Chronulac; Cillium; Cit http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202319.html
Levobetaxolol •
Ophthalmic - U.S. Brands: Betaxon; L-betaxolol http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500125.html
Losartan •
Systemic - U.S. Brands: Cozaar http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202767.html
Losartan and Hydrochlorothiazide •
Systemic - U.S. Brands: Hyzaar http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203639.html
Mecamylamine •
Systemic - U.S. Brands: Inversine http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202340.html
Methyldopa •
Systemic - U.S. Brands: Aldomet http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202359.html
Methyldopa and Thiazide Diuretics •
Systemic - U.S. Brands: Aldoclor; Aldoril http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202360.html
Metyrosine •
Systemic - U.S. Brands: Demser http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202368.html
394 Hypertension
Midodrine •
Systemic - U.S. Brands: ProAmatine http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203640.html
Minoxidil •
Systemic - U.S. Brands: Loniten http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202373.html
Nisoldipine •
Systemic - U.S. Brands: Sular http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203431.html
Phenoxybenzamine •
Systemic - U.S. Brands: Dibenzyline http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202458.html
Phenylpropanolamine •
Systemic - U.S. Brands: Note:; Propagest; Thinz-Span http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202462.html
Prazosin •
Systemic - U.S. Brands: Minipress http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202475.html
Prazosin and Polythiazide •
Systemic - U.S. Brands: Minizide http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202476.html
Rauwolfia Alkaloids •
Systemic - U.S. Brands: Harmonyl; Raudixin; Rauval; Rauverid; Serpalan; Wolfina http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202503.html
Rauwolfia Alkaloids and Thiazide Diuretics •
Systemic - U.S. Brands: Demi-Regroton; Diupres; Diurigen with Reserpine; Diutensen-R; Enduronyl; Enduronyl Forte; Oreticyl; Oreticyl Forte; Rauzide; Regroton http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202504.html
Reserpine, Hydralazine, and Hydrochlorothiazide •
Systemic - U.S. Brands: Cam-Ap-Es; Cherapas; Ser-A-Gen; Seralazide; Ser-ApEs; Serpazide; Tri-Hydroserpine; Unipres http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202506.html
Telmisartan •
Systemic - U.S. Brands: Micardis http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203710.html
Researching Medications 395
Terazosin •
Systemic - U.S. Brands: Hytrin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202546.html
Torsemide •
Systemic - U.S. Brands: Demadex http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202740.html
Trandolapril and Verapamil •
Systemic - U.S. Brands: Tarka http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203641.html
Unoprostone •
Ophthalmic - U.S. Brands: Rescula http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500199.html
Valsartan •
Systemic - U.S. Brands: Diovan http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203478.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/.
PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter,
396 Hypertension
Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee.
Researching Orphan Drugs Although the list of orphan drugs is revised on a daily basis, you can quickly research orphan drugs that might be applicable to hypertension by using the database managed by the National Organization for Rare Disorders, Inc. (NORD), at http://www.rarediseases.org/. Scroll down the page, and on the left toolbar, click on “Orphan Drug Designation Database.” On this page (http://www.rarediseases.org/search/noddsearch.html), type “hypertension” (or synonyms) into the search box, and click “Submit Query.” When you receive your results, note that not all of the drugs may be relevant, as some may have been withdrawn from orphan status. Write down or print out the name of each drug and the relevant contact information. From there, visit the Pharmacopeia Web site and type the name of each orphan drug into the search box at http://www.nlm.nih.gov/medlineplus/druginformation.html. You may need to contact the sponsor or NORD for further information. NORD conducts “early access programs for investigational new drugs (IND) under the Food and Drug Administration’s (FDA’s) approval ‘Treatment INDs’ programs which allow for a limited number of individuals to receive investigational drugs before FDA marketing approval.” If the orphan product about which you are seeking information is approved for marketing, information on side effects can be found on the product’s label. If the product is not approved, you may need to contact the sponsor. The following is a list of orphan drugs currently listed in the NORD Orphan Drug Designation Database for hypertension: •
Vapreotide (trade name: Octastatin) http://www.rarediseases.org/nord/search/nodd_full?code=1018
•
Bosentan (trade name: Tracleer) http://www.rarediseases.org/nord/search/nodd_full?code=1073
•
Nitric oxide http://www.rarediseases.org/nord/search/nodd_full?code=230
•
treprostinil (trade name: Remodulin) http://www.rarediseases.org/nord/search/nodd_full?code=1300
•
Epoprostenol (trade name: Flolan) http://www.rarediseases.org/nord/search/nodd_full?code=410
•
Beractant (trade name: Survanta Intratracheal Suspension) http://www.rarediseases.org/nord/search/nodd_full?code=591
•
CY-1503 (trade name: Cylexin) http://www.rarediseases.org/nord/search/nodd_full?code=694
•
15AU81 http://www.rarediseases.org/nord/search/nodd_full?code=871
Researching Medications 397
•
Beraprost http://www.rarediseases.org/nord/search/nodd_full?code=972
If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
399
APPENDICES
401
APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute13: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
•
National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
•
National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
•
National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
•
National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
•
National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
•
National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
•
National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
13
These publications are typically written by one or more of the various NIH Institutes.
402 Hypertension
•
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
•
National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
•
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
•
National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
•
National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
•
National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
•
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
•
National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
•
National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
•
National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
•
National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
•
National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
•
National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
•
Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
•
National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
•
National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
•
Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
•
Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
Physician Resources 403
NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.14 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:15 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
•
HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
•
NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
•
Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
•
Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
•
Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
•
Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
•
Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
•
Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
•
Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
•
MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
14
Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 15 See http://www.nlm.nih.gov/databases/databases.html.
404 Hypertension
•
Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
•
Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html The Combined Health Information Database
A comprehensive source of information on clinical guidelines written for professionals is the Combined Health Information Database. You will need to limit your search to one of the following: Brochure/Pamphlet, Fact Sheet, or Information Package, and “hypertension” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For the publication date, select “All Years.” Select your preferred language and the format option “Fact Sheet.” Type “hypertension” (or synonyms) into the “For these words:” box. The following is a sample result: •
Treatment of Hypertension: Insights from the JNC-VI Report Source: American Family Physician. 58(6): 1323-1330. October 15, 1998. Contact: Available from American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237. Website: www.aafp.org. Summary: This article summarizes the recommendations of the sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI) which provided updated guidelines for the treatment of hypertension. Antihypertensive drug therapy may be initiated either after a trial of lifestyle modifications or immediately after the diagnosis is made, depending on the patient's other cardiovascular risk factors and the presence of clinical cardiovascular disease. In general, therapy may begin with diuretics or beta adrenergic blockers in patients under age 65, unless a concomitant condition warrants another, more tailored choice. Low dosages should be used initially, but if the blood pressure is not successfully reduced to 140 over 90 mm Hg or below, another drug should be added or should replace the initial choice. General principles of therapy include the use of once a day formulations and combination drugs as well as cost considerations. 1 figure. 3 tables. 11 references. (AA-M).
•
National High Blood Pressure Education Program Working Group Report on Hypertension in Diabetes Source: Bethesda, MD: National Heart, Lung, and Blood Institute, National Institutes of Health. 1995. 26 p. Contact: Available from NHLBI Information Center. P.O. Box 30105, Bethesda, MD 20824-0105. (301) 251-1222. Fax (301) 251-1223. PRICE: $3.00; bulk discounts available. This publication is also available on the Internet at http://www.nhlbi.nih.gov/nhlbi/nhlbi.htm. Summary: This report is designed to increase awareness of the importance and implications of the problem of hypertension in persons with diabetes in community control programs; and to guide clinicians in their care of persons with the concomitant
Physician Resources 405
problems of hypertension and diabetes. Topics include definitions and diagnostic criteria; epidemiologic considerations; clinical trials; a guide to clinical evaluation; special considerations in patients with diabetes and hypertension, including kidney disease, secondary forms of hypertension, cardiovascular disease, cerebrovascular disease, diabetic retinopathy, hypertension with orthostatic hypotension, autonomic neuropathy, sexual dysfunction, lipid disorders, obesity, pregnancy, and children; treatment considerations, including lifestyle modifications, the pharmacologic treatment of hypertension, and drugs for managing hypertensive emergencies in patients with diabetes; and considerations in education, control, and maintenance. 3 figures. 116 references. (AA-M).
The NLM Gateway16 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.17 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “hypertension” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total
Items Found 225848 3878 340 334 84 230484
HSTAT18 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.19 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.20 Simply search by “hypertension” (or synonyms) at the following Web site: http://text.nlm.nih.gov. 16
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
17
The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 18 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 19 20
The HSTAT URL is http://hstat.nlm.nih.gov/.
Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse
406 Hypertension
Coffee Break: Tutorials for Biologists21 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.22 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.23 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
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Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
The Genome Project and Hypertension In the following section, we will discuss databases and references which relate to the Genome Project and hypertension. Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).24 The database contains textual Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations. 21 Adapted from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html. 22
The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 23 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process. 24 Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools
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information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “hypertension” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for hypertension: •
Arterial Occlusive Disease, Progressive, with Hypertension, Heart Defects, Bone Fragility, and Brachysyndactyly Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?602531
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Colonic Varices without Portal Hypertension Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?120440
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Diabetes Mellitus, Insulin-resistant, with Acanthosis Nigricans and Hypertension Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?604367
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Hypertension with Brachydactyly Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?112410
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Hypertension, Early-onset, Autosomal Dominant, with Severe Exacerbation in Pregnancy Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605115
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Hypertension, Essential Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?145500
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Hypertension, Essential, Susceptibility To, 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?603918
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Hypertension, Essential, Susceptibility To, 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?604329
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Hypertension, Essential, Susceptibility To, 3 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?607329
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Hypertension-associated Sa, Rat, Homolog of Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?145505
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Hypertensive Nephropathy Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?608026
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Intracranial Hypertension, Idiopathic Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?243200
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Osteochondrodysplasia, Rhizomelic, with Callosal Agenesis, Thrombocytopenia, Hydrocephalus, and Hypertension Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?166990
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Pulmonary Hypertension, Familial Persistent, of the Newborn Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?265380
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Pulmonary Hypertension, Primary Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?178600
for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.
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Pulmonary Hypertension, Primary Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?265400
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Renal Failure, Progressive, with Hypertension Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?161900
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Tachycardia, Hypertension, Microphthalmos, and Hyperglycinuria Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?272550 Genes and Disease (NCBI - Map)
The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed: •
Cancer: Uncontrolled cell division. Examples: Breast and ovarian cancer, Burkitt lymphoma, chronic myeloid leukemia, colon cancer, lung cancer, malignant melanoma, multiple endocrine neoplasia, neurofibromatosis, p53 tumor suppressor, pancreatic cancer, prostate cancer, Ras oncogene, RB: retinoblastoma, von Hippel-Lindau syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Cancer.html
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Immune System: Fights invaders. Examples: Asthma, autoimmune polyglandular syndrome, Crohn’s disease, DiGeorge syndrome, familial Mediterranean fever, immunodeficiency with Hyper-IgM, severe combined immunodeficiency. Web site: http://www.ncbi.nlm.nih.gov/disease/Immune.html
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Metabolism: Food and energy. Examples: Adreno-leukodystrophy, atherosclerosis, Best disease, Gaucher disease, glucose galactose malabsorption, gyrate atrophy, juvenile-onset diabetes, obesity, paroxysmal nocturnal hemoglobinuria, phenylketonuria, Refsum disease, Tangier disease, Tay-Sachs disease. Web site: http://www.ncbi.nlm.nih.gov/disease/Metabolism.html
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Muscle and Bone: Movement and growth. Examples: Duchenne muscular dystrophy, Ellis-van Creveld syndrome, Marfan syndrome, myotonic dystrophy, spinal muscular atrophy. Web site: http://www.ncbi.nlm.nih.gov/disease/Muscle.html
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Nervous System: Mind and body. Examples: Alzheimer disease, amyotrophic lateral sclerosis, Angelman syndrome, Charcot-Marie-Tooth disease, epilepsy, essential tremor, fragile X syndrome, Friedreich’s ataxia, Huntington disease, Niemann-Pick disease, Parkinson disease, Prader-Willi syndrome, Rett syndrome, spinocerebellar atrophy, Williams syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Brain.html
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Signals: Cellular messages. Examples: Ataxia telangiectasia, Cockayne syndrome, glaucoma, male-patterned baldness, SRY: sex determination, tuberous sclerosis, Waardenburg syndrome, Werner
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syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Signals.html •
Transporters: Pumps and channels. Examples: Cystic fibrosis, deafness, diastrophic dysplasia, Hemophilia A, long-QT syndrome, Menkes syndrome, Pendred syndrome, polycystic kidney disease, sickle cell anemia, Wilson’s disease, Zellweger syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Transporters.html Entrez
Entrez is a search and retrieval system that integrates several linked databases at the National Center for Biotechnology Information (NCBI). These databases include nucleotide sequences, protein sequences, macromolecular structures, whole genomes, and MEDLINE through PubMed. Entrez provides access to the following databases: •
3D Domains: Domains from Entrez Structure, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Books: Online books, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=books
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Genome: Complete genome assemblies, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome
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NCBI’s Protein Sequence Information Survey Results: Web site: http://www.ncbi.nlm.nih.gov/About/proteinsurvey/
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Nucleotide Sequence Database (Genbank): Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Nucleotide
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OMIM: Online Mendelian Inheritance in Man, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMIM
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PopSet: Population study data sets, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Popset
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ProbeSet: Gene Expression Omnibus (GEO), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Protein Sequence Database: Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Protein
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PubMed: Biomedical literature (PubMed), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
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Structure: Three-dimensional macromolecular structures, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Structure
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Taxonomy: Organisms in GenBank, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Taxonomy
To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then select the database that you would like to search. The databases available are listed in the drop box next to “Search.” Enter “hypertension” (or synonyms) into the search box and click “Go.”
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Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database25 This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html. The Genome Database26 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of scientific knowledge. Although GDB has historically focused on gene mapping, its focus will broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “hypertension” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).
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Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html. 26 Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission.
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on hypertension can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.
Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to hypertension. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly. The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below. Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to hypertension. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “hypertension”:
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Other guides Diabetes http://www.nlm.nih.gov/medlineplus/diabetes.html Glaucoma http://www.nlm.nih.gov/medlineplus/glaucoma.html Preeclampsia http://www.nlm.nih.gov/medlineplus/preeclampsia.html Respiratory Diseases http://www.nlm.nih.gov/medlineplus/respiratorydiseases.html Stroke http://www.nlm.nih.gov/medlineplus/stroke.html
Within the health topic page dedicated to hypertension, the following was listed: •
General/Overviews JAMA Patient Page: Lung Disease http://www.medem.com/MedLB/article_detaillb.cfm?article_ID=ZZZ06T60NAC &sub_cat=577 Lung Disease Source: National Women's Health Information Center http://www.4woman.gov/faq/lung_disease.htm
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Diagnosis/Symptoms Bronchoscopy: Pulmonary Branch Protocols http://www.cc.nih.gov/ccc/patient_education/pepubs/bronchoscopy.pdf Chest Pain, Acute: Self-Care Flowcharts Source: American Academy of Family Physicians http://familydoctor.org/flowcharts/523.html Radiography -- Chest (Chest X-ray) Source: American College of Radiology, Radiological Society of North America http://www.radiologyinfo.org/content/chest_radiography.htm Spirometry Source: National Lung Health Education Program http://www.nlhep.org/spirom1.html
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Coping Coping with Indoor Air Pollution Source: American Association for Respiratory Care http://www.aarc.org/patient_education/tips/inpoll.html Minimizing the Effects of Outdoor Air Pollution Source: American Association for Respiratory Care http://www.aarc.org/patient_education/tips/outpoll.html
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Traveling with Oxygen: Planning Is Key Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=HQ01555 •
Specific Conditions/Aspects Adult (Acute) Respiratory Distress Syndrome (ARDS) Source: American Lung Association http://www.lungusa.org/diseases/ards_factsheet.html Bronchiectasis Source: American Lung Association http://www.lungusa.org/diseases/bronchiectasis.html Collapsed Lung (Pneumothorax) Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=HQ01228 Goodpasture's Syndrome Source: National Kidney and Urologic Diseases Information Clearinghouse http://kidney.niddk.nih.gov/kudiseases/pubs/goodpasture/index.htm Hantavirus Pulmonary Syndrome Source: American Lung Association http://www.lungusa.org/diseases/hantavirus_factsheet.html Occupational Respiratory Diseases: Your Workplace and Your Lungs Source: American Academy of Family Physicians http://familydoctor.org/handouts/134.html Pleurisy Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00244 Primary Pulmonary Hypertension Source: National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/health/public/lung/other/pph_doc.htm Pulmonary Edema Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00412 Pulmonary Hypertension http://circ.ahajournals.org/cgi/reprint/106/24/e192.pdf Respiratory Failure http://www.nhlbi.nih.gov/health/public/lung/other/res_fail.pdf Spontaneous Pneumothorax Source: American Lung Association http://www.lungusa.org/diseases/pneumothorax.html
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Children Bronchopulmonary Dysplasia Source: National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/health/public/lung/other/bpd/toc.htm
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Helping Your Child Breathe Easier Source: American Association for Respiratory Care http://www.aarc.org/patient_education/tips/kids.html JAMA Patient Page: Your Child's Respiratory Health Source: American Medical Association http://www.medem.com/medlb/article_detaillb.cfm?article_ID=ZZZQOCATIAC &sub_cat=577 Looking at Your Lungs Source: Nemours Foundation http://kidshealth.org/kid/body/lungs_noSW.html Persistent Pulmonary Hypertension of the Newborn (PPHN) Source: Nemours Foundation http://kidshealth.org/parent/medical/heart/pphn.html Primary Ciliary Dyskinesia Source: American Lung Association http://www.lungusa.org/diseases/pcd.html Respiratory Distress Syndrome of the Newborn Source: American Lung Association http://www.lungusa.org/diseases/rdsfac.html Transient Tachypnea of the Newborn (TTN) Source: Nemours Foundation http://kidshealth.org/parent/medical/lungs/ttn.html •
From the National Institutes of Health Lungs in Health and Disease http://www.nhlbi.nih.gov/health/public/lung/other/lungs_hd.pdf
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Latest News Enzyme Deficiency Testing Urged for Lung Patients Source: 10/17/2003, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_14321 .html Study Tracks Asthma's Roots to Childhood Source: 10/09/2003, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_14242 .html Sunken Chest Affects Aerobic Fitness Source: 10/13/2003, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_14271 .html
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Men Facts About Lymphangioleiomyomatosis (LAM) Source: National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/health/public/lung/other/lam.htm
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Organizations American College of Chest Physicians http://www.chestnet.org/ American Lung Association http://www.lungusa.org/ National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/ National Institute of Allergy and Infectious Diseases http://www.niaid.nih.gov/ National Lung Health Education Program http://www.nlhep.org/
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Pictures/Diagrams Atlas of the Body: The Respiratory System -- Structure Detail Source: American Medical Association http://www.medem.com/MedLB/article_detaillb.cfm?article_ID=ZZZ8PPLCGJC &sub_cat=285 How the Body Works: The Respiratory System Source: Nemours Foundation http://kidshealth.org/misc_pages/bodyworks/resp.html
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Research Are Beta-1-Blockers Safe for Patients with Lung Disease? Source: American College of Physicians http://www.annals.org/cgi/content/full/137/9/I-31 Myocarditis Plus Pulmonary Hypertension Means Transplant Sooner Source: American Heart Association http://www.americanheart.org/presenter.jhtml?identifier=3001358 Sildenafil (Viagra) May Help Improve Control of Pulmonary Hypertension Source: American College of Physicians http://www.annals.org/cgi/content/full/136/7/I35
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Statistics African Americans and Lung Disease Source: American Lung Association http://www.lungusa.org/diseases/africanlung_factsheet.html American Indians/Alaskan Natives and Lung Disease Source: American Lung Association http://www.lungusa.org/diseases/nativelung_factsheet.html Asian Americans/Pacific Islanders and Lung Disease Source: American Lung Association http://www.lungusa.org/diseases/asianlung_factsheet.html
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Hispanics and Lung Disease Source: American Lung Association http://www.lungusa.org/diseases/hispaniclung_factsheet.html Minority Lung Disease Data 2000 Source: American Lung Association http://www.lungusa.org/pub/minority/mldd_00.html New Edition of Lung Disease Data Report Updates Resource with Newest Available Statistics Source: National Institute for Occupational Safety and Health http://www.cdc.gov/niosh/worldre02.html Pulmonary Hypertension Source: National Center for Chronic Disease Prevention and Health Promotion http://www.cdc.gov/cvh/library/fs_pulmonary_hypertension.htm State-by-State Lung Disease Trend Report April 2001 Source: American Lung Association http://www.lungusa.org/data/s2s/s2s_index.html •
Women Facts About Lymphangioleiomyomatosis (LAM) Source: National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/health/public/lung/other/lam.htm
You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on hypertension. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: •
Hypertension Source: Lenexa, KS: North American Transplant Coordinators Organization. 199x. 2 p. Contact: Available from North American Transplant Coordinators Organization. P.O. Box 15384, Lenexa, KS 66285-5384. (913) 492-3600. PRICE: $0.25. Summary: This brief brochure answers questions about hypertension (high blood pressure) commonly asked by patients undergoing kidney transplantation. Topics include a definition of blood pressure and hypertension; factors that contribute to
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hypertension, including obesity, eating too much salt, smoking, drinking alcohol, certain medications, psychological stress, gout, pregnancy, diabetes, heredity, and kidney disease; the complications of hypertension; the symptoms of hypertension (often there are none); and posttransplant changes in hypertension. The brochure concludes with a discussion of antihypertensive medications and other treatment options, including lifestyle changes. The brochure emphasizes that hypertension can cause the loss of a transplanted kidney, just as it can cause damage and loss of native kidneys. The brochure includes the address and telephone number of the North American Transplant Coordinators Organization. •
When Hypertension Is Not the Only Problem: Hypertension and Diabetes Mellitus Source: Wayne, PA: Astra Merck. 1996. 4 p. Contact: Available from Astra Merck Information Center. 725 Chesterbrook Boulevard, Wayne, PA 19087-5677. (800) 236-9933 or (610) 695-1000. PRICE: Single copy free. Summary: This brochure familiarizes readers with hypertension and how it can be complicated by diabetes. The brochure describes the systolic and diastolic numbers of the blood pressure, and defines hypertension. The author defines diabetes and notes the importance of blood glucose control and the impact of hypertension on blood glucose control. Other topics include risk factors for hypertension, including age, race, salt intake, body weight, and gender factors; drug therapy for hypertension; and ways to reduce cardiovascular risks by changes in everyday activities. The brochure concludes with a blank page for the reader or physician to record comments and individualized instructions. The brochure features bold, colorful graphics. 1 figure.
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Hypertension Nutrition Recommendations Source: West Hills, CA: Nutrition Prescriptives. 1997. 1 p. Contact: Available from Nutrition Prescriptives. P.O. Box 4417, West Hills, CA 91308. (818) 347-4760. Fax (818) 992-4319. E-mail:
[email protected]. PRICE: $10.00. Summary: This copier-ready, interactive counseling tool is designed to help health care professionals educate patients about the relationship between nutrition and hypertension. The fact sheet provides an action plan for reducing sodium intake, reaching and maintaining a reasonable body weight, drinking less alcohol, choosing foods rich in potassium and calcium, and exercising regularly. Space is provided for patients to personalize the suggestions given. The fact sheet includes several computergenerated illustrations and is printed on durable stock. Purchase of a master fact sheet includes a non-transferable license to make copies for patients. (AA-M).
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Pulmonary Hypertension and HIV Contact: Project Inform, National HIV/AIDS Treatment Hotline, 205 13th St Ste 2001, San Francisco, CA, 94103, (415) 558-8669, http://www.projectinform.org. Summary: This information sheet, for individuals with the human immunodeficiency syndrome (HIV)/acquired immune deficiency syndrome (AIDS), provides information about pulmonary hypertension (PH) and its relationship to HIV/AIDS. The information sheet discusses PH symptoms, how PH affects HIV-positive persons, and available treatments for persons with HIV/AIDS.
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Pulmonary Hypertension Source: Danvers, MA: Scleroderma Foundation. 1998. 6 p. Contact: Available from Scleroderma Foundation. 12 Kent Way, Suite 101, Byfield, MA 01922. (800) 722-4673 or (978) 463-5843. Fax (978) 463-5809. E-mail:
[email protected]. Website: www.scleroderma.org. PRICE: Single copy $1.00. Summary: This pamphlet for people with scleroderma uses a question and answer format to provide information about pulmonary artery hypertension. This type of high blood pressure involves the arteries that take blood from the right side of the heart to the lungs. The pamphlet describes the types of pulmonary artery hypertension that occur in scleroderma, including hypertension with or without scarring of the lung tissue. It also presents the symptoms of pulmonary artery hypertension, highlights the tests that might be conducted to diagnose pulmonary artery hypertension, explains the natural course of this condition in scleroderma, and discusses options for treating this type of hypertension. Pulmonary hypertension not related to scleroderma may be treated with oxygen therapy and anticoagulation therapy. Right-heart failure may be treated with various medications, including calcium channel blockers, diuretics, and an experimental drug known as prostacyclin. In addition, the pamphlet presents the mission of the Scleroderma Foundation.
The National Guideline Clearinghouse™ The National Guideline Clearinghouse™ offers hundreds of evidence-based clinical practice guidelines published in the United States and other countries. You can search this site located at http://www.guideline.gov/ by using the keyword “hypertension” (or synonyms). The following was recently posted: •
Diagnosis and management of hypertension in the primary care setting Source: Department of Defense - Federal Government Agency [U.S.]; 1999 May; Various pagings http://www.guideline.gov/summary/summary.aspx?doc_id=2579&nbr=1805&a mp;string=hypertension
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Essential hypertension Source: University of Michigan Health System - Academic Institution; 1997 (revised 2002 Aug); 14 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3539&nbr=2765&a mp;string=hypertension
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Hypertension Source: National Committee on Cardiac Care (Singapore) - National Government Agency [Non-U.S.]; 2000 December; 42 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2837&nbr=2063&a mp;string=hypertension
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Hypertension Source: University of Texas Medical Branch Correctional Managed Care - Academic Institution; 1997 March (revised 2002 Apr); 6 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3475&nbr=2701&a mp;string=hypertension
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Hypertension in older people. A national clinical guideline Source: Scottish Intercollegiate Guidelines Network - National Government Agency [Non-U.S.]; 2001 January; 49 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2915&nbr=2141&a mp;string=hypertension
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Nutritional strategies efficacious in the prevention or treatment of hypertension Source: Nutrition Screening Initiative - Professional Association; 1998; 15 pages http://www.guideline.gov/summary/summary.aspx?doc_id=1417&nbr=590&am p;string=hypertension
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Primary prevention of hypertension. Clinical and public health advisory from the National High Blood Pressure Education Program Source: National Heart, Lung, and Blood Institute (U.S.) - Federal Government Agency [U.S.]; 1993 (revised 2002 October 16); 7 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3482&nbr=2708&a mp;string=hypertension
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Procedure guideline for diagnosis of renovascular hypertension Source: Society of Nuclear Medicine, Inc - Medical Specialty Society; 1999 February; 20 pages http://www.guideline.gov/summary/summary.aspx?doc_id=1359&nbr=617&am p;string=hypertension
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Screening for hypertension in adults Source: University of Texas at Austin School of Nursing, Family Nurse Practitioner Program - Academic Institution; 2002 May; 9 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3226&nbr=2452&a mp;string=hypertension
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Treatment of hypertension in adults with diabetes Source: American Diabetes Association - Professional Association; 2001 October (republished 2003 Jan); 3 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3573&nbr=2799&a mp;string=hypertension
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Healthfinder™ Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database: •
Age Page - High Blood Pressure--A Common but Controllable Disorder Summary: This pamphlet provides basic facts about high blood pressure (hypertension)-what it is, how it is tested, what causes it, and how it can be treated, controled and prevented. Source: National Institute on Aging, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=36
•
Hypertension (Journal) Summary: One of five monthly Journals for the public and healthcare professional published by the American Heart Association. Source: American Heart Association http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=1948
•
Pulmonary Hypertension Support Groups Summary: An online listing of national and international pulmonary hypertension support groups provided as a service to patients and their families by the Pulmonary Hypertension Association. Source: Pulmonary Hypertension Association http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=5609 The NIH Search Utility
The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to hypertension. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources
A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
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•
Family Village: http://www.familyvillage.wisc.edu/specific.htm
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Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
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Med Help International: http://www.medhelp.org/HealthTopics/A.html
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Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
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Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
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WebMDHealth: http://my.webmd.com/health_topics
Associations and Hypertension The following is a list of associations that provide information on and resources relating to hypertension: •
Addison and Cushing International Federation Telephone: 31-153699339 Fax: 31-153699339 Email:
[email protected] Web Site: www.nvacp.nl Background: The Addison and Cushing International Federation (ACIF), established in 1996, is a platform of organisations involved in the support of those affected with Addison's disease, Cushing's syndrome (or disease) and related adrenal or pituitaryrelated diseases (e.g., Acromegaly, CAH and other disorders). ACIF maintains a listing of organisations, support groups and individuals who want to start support groups in countries where none exist, that are involved in the field of adrenal and pituitary disorders. The ACIF web site remains a part of the web site of the Dutch Addison and Cushing Society (NVACP). Whenever possible, messages will be diverted to existing patient support groups already known to ACIF. Addison's disease is a rare disorder characterized by deficiency of certain hormones (i.e., hydrocortisone and aldosterone) produced by the outer region (cortex) of the adrenal glands. Acute episodes (Addisonian crises) may be characterized by excessive loss of sodium and water in the urine, dehydration, low blood pressure (hypotension), extreme muscle weakness, confusion, and coma. In most cases, however, the disease's onset is chronic and progressive where affected individuals may experience fatigue, weakness, weight loss, abdominal pain, and abnormal darkening of the skin in certain areas of the body. Cushing's syndrome is a hormonal disorder characterized by abnormally increased levels of certain hormones (i.e., corticosteroid hormones) produced by the adrenal glands. Associated symptoms and findings may include abnormal roundness and reddening of the face, weight gain, wasting of the limbs, excessive hair growth, loss of bone density and susceptibility to fractures (osteoporosis), increased blood pressure (hypertension), susceptibility to bruising, mental changes, and/or other abnormalities.
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Alveolar Capillary Dysplasia Association Telephone: (630) 416-6776 Fax: (630) 416-6776 Email:
[email protected] Web Site: http://www.acd-association.com
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Background: The Alveolar Capillary Dysplasia Association is a not-for-profit organization dedicated to providing information, support, and resources to parents of children born with alveolar capillary dysplasia (ACD). ACD is a condition characterized by abnormal development (dysplasia) of the tiny air sacs in the lungs (alveoli). In all reported cases, ACD has occurred in association with primary pulmonary hypertension of the newborn (PPHN), which is characterized by abnormally increased blood pressure in the arteries supplying the lungs. Affected infants also typically have misalignment of pulmonary veins, poor development of certain capillaries, and/or other findings. In most cases, during the first days of life, affected newborns develop a bluish discoloration of the skin and mucous membranes (cyanosis) due to abnormally low levels of circulating oxygen (hypoxia) and experience difficulty breathing. In many cases, life-threatening complications may result within approximately three to four weeks. The condition usually appears to occur randomly, for no apparent reason (sporadic). However, a few familial cases have been reported. The Alveolar Capillary Dysplasia Association was established in 1997 by the parents of a child born with ACD. The Association is committed to providing mutual support to affected families through networking services; offering information concerning current research; educating the medical community and the general public about alveolar capillary dysplasia; and working with affected families and the medical community to expand the current knowledge of ACD. The Association offers an in-depth bibliography of medical journal articles on ACD, provides a newsletter via e-mail, and has a web site on the Internet that offers understandable information on ACD, a guestbook area, and linkage to additional sources of information and support. •
American Council of the Blind, Inc Telephone: (202) 467-5081 Toll-free: (800) 424-8666 Fax: (202) 467-5085 Email:
[email protected] Web Site: http://www.acb.org Background: The American Council of the Blind is a national not-for-profit advocacy organization for people who are blind or visually impaired. Established in 1961, the Council is dedicated to improving the well-being of all blind and visually impaired people. To this end, the Council serves as a representative national organization and seeks to improve the social, economic, and cultural levels of affected individuals. The Council is dedicated to improving educational and rehabilitation opportunities and cooperating with public and private institutions and organizations concerned with services for people who are blind. The Society produces a variety of publications including the 'Braille Forum.' Produced in Braille, large print, four track cassette, and on computer disk, the magazine contains articles on employment, legislation, sports and leisure activities, new products and services, human interest stories, and other information. The Society also supports a national toll-free information and referral service.
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American Foundation for the Blind Telephone: (212) 502-7600 Toll-free: (800) 232-5463 Fax: (212) 502-7777 Email:
[email protected] Web Site: http://www.afb.org
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Background: The American Foundation for the Blind (AFB) is a national not-for-profit voluntary organization established in 1921 and recognized as Helen Keller s cause in the United States. AFB is the leading national resource for people who are blind or visually impaired, the organizations that serve them, and the general public. The mission of AFB is to enable people who are blind or visually impaired to achieve equality of access and opportunity that will ensure freedom of choice in their lives. AFB fulfills this mission through four primary areas of activity regarding the non-medical aspects of blindness and visual impairment. These include: the development, collection and dissemination of information on blindness and visual impairment; identification, analysis, and resolution of critical issues related to blindness and visual impairment; education of the public and policy makers as to the needs and capabilities of people who are blind or visually impaired; and the production and distribution of talking books and other audio materials. AFB records and duplicates talking books under contract to the Library of Congress and publishes books, pamphlets, videos, and periodicals about blindness for professionals and health care consumers. In addition, AFB publishes the 'Journal of Visual Impairment and Blindness.'. •
American Heart Association Telephone: (214) 373-6300 Toll-free: (800) 242-8721 Fax: (214) 373-0268 Email:
[email protected] Web Site: http://www.americanheart.org Background: The American Heart Association (AHA), a national not-for-profit voluntary health agency funded by private contributions, is dedicated to the reduction of death and disability from cardiovascular diseases including heart diseases and stroke. The Association consists of approximately 2,000 community organizations in all states, the District of Columbia, and Puerto Rico. More than 4 million people volunteer with the Association to fight cardiovascular diseases, the nation s number one cause of death and leading cause of disability. Preventing heart disease and stroke is the first priority of the American Heart Association. In support of this goal, the Association has contributed more than one billion dollars to cardiovascular research since 1949. The Association also distributes a variety of educational materials and sponsors continuing medical education (CME) seminars and meetings.
•
Intracranial Hypertension Research Foundation (IHRF) Telephone: (360) 693-4473 Fax: (360) 694-7062 Email:
[email protected] Web Site: www.http://www.ihrfoundation.org Background: The Intracranial Hypertension Research Foundation (IHRF) was formed to sponsor the development of new research on the causes of intracranial hypertension syndrome and to develop treatments and, ultimately, a cure. Its mission includes identifying and removing barriers to the implementation of such therapies. Intracranial hupertension is a general name for the disorders in which the cerebrospinal fluid pressure within the skull is too high. It often leads to loss of vision, blindness, and significant neurological difficulties. IHRF assists in the identification of research opportunities. It encourages the exchange of information through symposia, medical
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meetings, and the Internet. Newsletters and other printed materials also are used to disseminate information. •
March of Dimes Birth Defects Foundation Telephone: (914) 428-7100 Toll-free: (888) 663-4637 Fax: (914) 997-4763 Email:
[email protected] Web Site: http://www.marchofdimes.com Background: The March of Dimes Birth Defects Foundation is a national not-for-profit organization that was established in 1938. The mission of the Foundation is to improve the health of babies by preventing birth defects and infant mortality. The March of Dimes funds programs of research, community services, education, and advocacy. Educational programs that seek to prevent birth defects are important to the Foundation and to that end it also produces a wide variety of printed informational materials and videos. The Pregnancy and Newborn Health Education Center staffs trained health information specialists who provide researched information on pregnancy issues, complications and risks, newborn care, birth defects, genetic diseases and related topics as well as referrals to relevant organizations and support groups.
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National Association for Visually Handicapped Telephone: (212) 889-3141 Fax: (212) 727-2931 Email:
[email protected] Web Site: http://www.navh.org Background: The National Association for Visually Handicapped provides emotional support, visual aids, technology and training to visually impaired children, adults, and seniors. Founded in 1954, NAVH has helped hundreds of thousands of the 'hard of seeing' resume independent, more productive, more dignified lives among their fully sighted peers. The organization also promotes the publication of educational materials and their distribution to schools, libraries, social institutions, and individuals. The Association seeks to plan and assist in programs of parent and adult education relating to persons with partial seeing and to assist and encourage the partially seeing to integrate into the mainstream of society. To this end, NAVH, publishes brochures, a publications listing, and other notices.
•
National Eye Research Foundation Telephone: (847) 564-4652 Toll-free: (800) 621-2258 Fax: (847) 564-0807 Email:
[email protected] Web Site: http://www.nerf.org Background: The National Eye Research Foundation (NERF) is a nonprofit, international organization dedicated to improving eye care for the public and meeting the professional needs of eye care practitioners. The Foundation sponsors eye research projects on contact lens applications and eye care problems. Established in 1955, NERF is committed to professional enrichment through special study sections in such fields as
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orthokeratology, primary eye care, pediatrics, and through continuing education programs. The Foundation provides eye care information for the public and professionals. Consisting of 300 members, the organization produces educational materials including a pamphlet series. Program activities include education and referrals. •
National Hypertension Association, Inc Telephone: (212) 889-3557 Toll-free: (800) 575-9355 Fax: (212) 447-7032 Background: The National Hypertension Association, Inc. (NHA) is a not-for-profit organization dedicated to combating the chronic health problem of high blood pressure (hypertension) by developing, directing, and implementing effective programs to promote research, educate the public, and ensure prompt detection and effective treatment of hypertension. The NHA is committed to researching the causes of essential hypertension and enhancing the understanding of certain secondary types of hypertension through basic laboratory research studies, thereby improving treatment of these conditions; educating and alerting the public to the severe, life-threatening dangers of hypertension and informing physicians as well as medical students of the most current advances in its causes, diagnosis, treatment, and prevention; and detecting hypertension wherever it exists in the most economical and effective way and urging treatment if indicated. Established in 1977 by a group of concerned scientists, doctors, and philanthropists, NHA offers charitable blood pressure screening, provides work-site detection programs, and has a well-defined program of basic and clinical research to gain better insight into the causes of hypertension. Materials include brochures, pamphlets, a regular newsletter, reports, and information packets. Relevant area(s) of interest: Hypertension
•
Pseudotumor Cerebri Support Network Telephone: (614) 794-0442 Fax: (614) 837-5913 Web Site: http://www.pseudotumorcerebri.com Background: The Pseudotumor Cerebri (PTC) Support Network is a national non-profit support organization dedicated to supporting research, treatment, and medical care of individuals who are diagnosed with pseudotumor cerebri. Pseudotumor cerebri is a syndrome of increased pressure inside the skull. It is most often seen in obese females between the ages of 20 and 50 years. Symptoms can mimic those of a brain tumor; however, no tumor is involved. Established in 1992, the PCT Network publishes a periodic newsletter to help keep individuals with pseudotumor cerebri informed of current treatments and ongoing research.
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Pulmonary Hypertension Association Telephone: (301) 565-3004 Toll-free: (800) 748-7274 Fax: (301) 565-3994 Email:
[email protected] Web Site: http://www.phassociation.org
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Background: The Pulmonary Hypertension Association (PHA) is an international notfor-profit voluntary organization that provides educational information and fellowship to people with primary or secondary pulmonary hypertension. Pulmonary hypertension is a condition characterized by abnormally high blood pressure in the arteries that supply the lungs. Pulmonary hypertension may be an isolated condition that may occur for unknown reasons (primary pulmonary hypertension) or may occur due to or in association with other underlying disorders or conditions (secondary pulmonary hypertension). Established in 1992, the organization addresses issues pertinent to people with these disorders such as current research, early detection, orphan drug designations, organ donor awareness, and organ transplantation. It conducts international conferences; provides a networking service; offers referrals; and publishes a quarterly newsletter, 'Pathlight.'. •
Schepens Eye Research Institute Telephone: (617) 912-0100 Fax: (617) 523-3463 Email:
[email protected] Web Site: http://www.eri.harvard.edu Background: The Schepens Eye Research Institute, a not-for-profit organization, is a prominent center for research on the eye, vision, and blinding diseases. Established in 1950 and an affiliate of the Department of Ophthalmology at Harvard Medical School, the Schepens Eye Research Institute is dedicated to research that improves the understanding, management, and prevention of eye diseases and visual deficiencies; fosters collaboration among its faculty members; trains young scientists and clinicians from around the world; promotes communication with scientists in allied fields; and is a leader in the worldwide dispersion of basic scientific knowledge of vision. The Schepens Eye Research Institute's research program focuses on eye studies and the search for causes of disease in several core areas, including retinal and macular diseases (macular degeneration and diabetic retinopathy), corneal and ocular surface diseases (dry eye syndrome and corneal infection and injury), anterior segment diseases (glaucoma), ocular immunology (ocular cancer, inflammation, viral infections), transplantation (retinal and corneal transplants), and low vision aids and diagnostic technologies. The Schepens Eye Research Institute provides a variety of materials including brochures, reports and a magazine.
•
Second Wind Lung Transplant Association, Inc Telephone: Toll-free: (888) 222-2690 Fax: (727) 442-9762 Email:
[email protected] Web Site: http://www.2ndwind.org Background: Second Wind Lung Transplant Association, Inc. is a not-for-profit organization dedicated to improving the quality of life for lung transplant recipients, lung surgery candidates, people with related pulmonary concerns, and their families. The Association provides support, advocacy, education, information, and guidance through a spirit of service, 'adding years to their lives and life to their years.' Established in 1995 by a group of lung transplant recipients, candidates, and their families, Second Wind has quarterly support group meetings to provide educational programs (e.g., on
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nutrition, effects of medications and exercise, physical therapy) for both lung transplant candidates and recipients; to share experiences; and to enjoy social activities. In addition, the organization provides educational programs; seeks to increase Organ Donor Awareness; and provides a quarterly newsletter entitled 'AirWays' to its members.
Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to hypertension. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with hypertension. The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about hypertension. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “hypertension” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “hypertension”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For
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publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “hypertension” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “hypertension” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.27
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
27
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)28: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
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Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
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Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
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California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
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California: Gateway Health Library (Sutter Gould Medical Foundation)
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California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
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California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
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California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
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California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
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California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
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Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
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Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
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Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
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Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
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Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
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Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
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Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
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Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
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Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
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Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
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Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
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Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
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Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
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Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
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Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
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Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
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Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
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Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
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Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
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Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
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Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
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Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
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Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
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Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
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Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
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Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
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Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
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Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
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Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
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Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
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Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
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Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
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Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
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Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
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National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
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National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
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National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
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MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
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Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
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On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
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Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
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Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on hypertension: •
Basic Guidelines for Hypertension Coarctation of the aorta Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000191.htm Essential hypertension Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000153.htm Hypertension Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000468.htm Hypertensive heart disease Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000163.htm Hypertensive intracerebral hemorrhage Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000715.htm Hypertensive retinopathy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000999.htm
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Pheochromocytoma Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000340.htm Renal hypertension Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000204.htm Renovascular hypertension Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000204.htm •
Signs & Symptoms for Hypertension Abnormal sensations Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003206.htm Anxiety Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003211.htm Chest pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003079.htm Comatose Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003202.htm Confusion Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003205.htm Cough Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003072.htm Coughing Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003072.htm Decreased consciousness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003202.htm Decreased sensation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003206.htm Decreased vision Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003029.htm Difficulty breathing Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003075.htm Difficulty speaking Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003204.htm Difficulty swallowing Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003115.htm
Online Glossaries 437
Dizziness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003093.htm Ear noise/buzzing Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003043.htm Edema Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm Excessive perspiration Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003218.htm Faintness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003092.htm Fatigue Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm Headache Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003024.htm Headaches Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003024.htm Heartbeat sensations Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003081.htm High blood pressure Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003082.htm Inability to speak Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003204.htm Increased frequency of urination at night Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003141.htm Irregular pulse Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003081.htm Lethargic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm Loss of balance Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003093.htm Loss of consciousness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003202.htm Loss of coordination Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003198.htm
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Loss of vision Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003040.htm Muscle Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003193.htm Nausea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003117.htm Nosebleed - symptom Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003106.htm Numbness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003206.htm Obesity Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003101.htm Overweight Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003101.htm Pale skin Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003244.htm Palpitations Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003081.htm Seizure Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003200.htm Seizures Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003200.htm Shortness of breath Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003075.htm Sleepy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003208.htm Splenomegaly Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003276.htm Stria Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003287.htm Stuporous Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003202.htm Swallowing difficulties Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003115.htm
Online Glossaries 439
Sweating Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003218.htm Swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm Swelling of the feet Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003104.htm Tingling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003206.htm Tiredness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm Visual disturbances Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003029.htm Vomiting Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003117.htm Waking at night short of breath Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003076.htm Weakness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003174.htm Weight loss Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003107.htm •
Diagnostics and Tests for Hypertension Alpha-1 antitrypsin Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003715.htm ALT Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003473.htm Angiography of the head Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003799.htm Bleeding time Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003656.htm Blood pressure Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003398.htm BUN Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003474.htm
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CBC Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003642.htm Chest CT scan Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003788.htm Chest X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003804.htm Coronary angiogram Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003876.htm Creatinine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003475.htm Diastolic blood pressure Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003398.htm ECG Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003868.htm Echocardiogram Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003869.htm Fluorescein angiography Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003846.htm HDL Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003496.htm Head CT scan Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003786.htm Head MRI Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003791.htm Liver function tests Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003436.htm Liver scan Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003825.htm Metanephrine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003613.htm Ophthalmoscopic examination Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003881.htm Ophthalmoscopy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003881.htm
Online Glossaries 441
Partial thromboplastin time Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003653.htm Platelet count Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003647.htm Prothrombin time Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003652.htm RBC count Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003644.htm Systolic blood pressure Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003398.htm Ultrasound Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003336.htm Uric acid Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003476.htm Urinalysis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003579.htm Visual field Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003879.htm •
Nutrition for Hypertension Cholesterol Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002472.htm Fats Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002468.htm Sodium in diet Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002415.htm
•
Surgery and Procedures for Hypertension Angioplasty Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002953.htm Shunt Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003019.htm
•
Background Topics for Hypertension Analgesics Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002123.htm
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Bleeding Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000045.htm Calcium antagonists Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002580.htm Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Endocrine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002351.htm Enzyme Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002353.htm Exercise Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001941.htm Heart disease Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000147.htm Incidence Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002387.htm Kidney function tests Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003435.htm Renal Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002289.htm Retina Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002291.htm Smoking Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002032.htm Strain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000042.htm Systemic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002294.htm Unconscious Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000022.htm
Online Glossaries 443
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
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MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
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Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
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Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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HYPERTENSION DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 1-Phosphatidylinositol 3-Kinase: An enzyme that catalyzes the conversion of phosphatidylinositol to phosphatidylinositol 3-phosphate. This is the first committed step in the biosynthesis of phosphatidylinositol 3,4-bisphosphate and phosphatidylinositol 3,4,5trisphosphate. This pathway is thought to play a critical role in DNA repair, V(D)J recombination and cell cycle checkpoints. EC 2.7.1.137. [NIH] Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal fat: Fat (adipose tissue) that is centrally distributed between the thorax and pelvis and that induces greater health risk. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Ablation: The removal of an organ by surgery. [NIH] Abscess: Accumulation of purulent material in tissues, organs, or circumscribed spaces, usually associated with signs of infection. [NIH] Acatalasia: A rare autosomal recessive disorder resulting from the absence of catalase activity. Though usually asymptomatic, a syndrome of oral ulcerations and gangrene may be present. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acetic Acids: Acetic acid and its derivatives which may be formed by substitution reactions. Mono- and di-substituted, as well as halogenated compounds have been synthesized. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acidosis: A pathologic condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, and characterized by an increase in hydrogen ion concentration. [EU] Acne: A disorder of the skin marked by inflammation of oil glands and hair glands. [NIH] Acrylonitrile: A highly poisonous compound used widely in the manufacture of plastics, adhesives and synthetic rubber. [NIH] Actin: Essential component of the cell skeleton. [NIH] Acute lymphoblastic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphocytic leukemia. [NIH]
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Acute lymphocytic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphoblastic leukemia. [NIH] Acute renal: A condition in which the kidneys suddenly stop working. In most cases, kidneys can recover from almost complete loss of function. [NIH] Acyl: Chemical signal used by bacteria to communicate. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenoma: A benign epithelial tumor with a glandular organization. [NIH] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenosine Triphosphate: Adenosine 5'-(tetrahydrogen triphosphate). An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter. [NIH] Adenosinetriphosphatase: A group of enzymes which catalyze the hydrolysis of ATP coupled with another function such as transporting Ca(2+) across a membrane. These enzymes may be dependent on Ca(2+), Mg(2+), anions, H+, or DNA. EC 3.6.1.3. [NIH] Adenovirus: A group of viruses that cause respiratory tract and eye infections. Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH] Adipocytes: Fat-storing cells found mostly in the abdominal cavity and subcutaneous tissue. Fat is usually stored in the form of tryglycerides. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adjunctive Therapy: Another treatment used together with the primary treatment. Its purpose is to assist the primary treatment. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Glands: Paired glands situated in the retroperitoneal tissues at the superior pole of each kidney. [NIH] Adrenal Medulla: The inner part of the adrenal gland; it synthesizes, stores and releases catecholamines. [NIH]
Dictionary 447
Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adrenergic Agonists: Drugs that bind to and activate adrenergic receptors. [NIH] Adrenergic Antagonists: Drugs that bind to but do not activate adrenergic receptors. Adrenergic antagonists block the actions of the endogenous adrenergic transmitters epinephrine and norepinephrine. [NIH] Adrenergic beta-Antagonists: Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic betaantagonists are used for treatment of hypertension, cardiac arrythmias, angina pectoris, glaucoma, migraine headaches, and anxiety. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aerobic Exercise: A type of physical activity that includes walking, jogging, running, and dancing. Aerobic training improves the efficiency of the aerobic energy-producing systems that can improve cardiorespiratory endurance. [NIH] Aerobic Metabolism: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as aerobic respiration, oxidative metabolism, or cell respiration. [NIH] Aerobic Respiration: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as oxidative metabolism, cell respiration, or aerobic metabolism. [NIH] Aerosol: A solution of a drug which can be atomized into a fine mist for inhalation therapy. [EU]
Aetiology: Study of the causes of disease. [EU] Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Afferent Pathways: Nerve structures through which impulses are conducted from a peripheral part toward a nerve center. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Afterload: The tension produced by the heart muscle after contraction. [EU] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
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Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [NIH] Ageing: A physiological or morphological change in the life of an organism or its parts, generally irreversible and typically associated with a decline in growth and reproductive vigor. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Air Sacs: Thin-walled sacs or spaces which function as a part of the respiratory system in birds, fishes, insects, and mammals. [NIH] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Alanine: A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system. [NIH] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Albuminuria: More than normal amounts of a protein called albumin in the urine. Albuminuria may be a sign of kidney disease. [NIH] Aldehydes: Organic compounds containing a carbonyl group in the form -CHO. [NIH] Aldosterone: (11 beta)-11,21-Dihydroxy-3,20-dioxopregn-4-en-18-al. A hormone secreted by the adrenal cortex that functions in the regulation of electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkaline: Having the reactions of an alkali. [EU] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alkalosis: A pathological condition that removes acid or adds base to the body fluids. [NIH] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allograft: An organ or tissue transplant between two humans. [NIH] Allopurinol: A xanthine oxidase inhibitor that decreases uric acid production. [NIH] Allylamine: Possesses an unusual and selective cytotoxicity for vascular smooth muscle cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial
Dictionary 449
fibrosis or cardiac decompensation. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alpha-1: A protein with the property of inactivating proteolytic enzymes such as leucocyte collagenase and elastase. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Aluminum: A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98. [NIH] Alveolar Process: The thickest and spongiest part of the maxilla and mandible hollowed out into deep cavities for the teeth. [NIH] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Ameliorated: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric acid, that have no relation to proteins. Abbreviated AA. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acid Substitution: The naturally occurring or experimentally induced replacement of one or more amino acids in a protein with another. If a functionally equivalent amino acid is substituted, the protein may retain wild-type activity. Substitution may also diminish or eliminate protein function. Experimentally induced substitution is often used to study enzyme activities and binding site properties. [NIH] Amlodipine: 2-((2-Aminoethoxy)methyl)-4-(2-chlorophenyl)-1,4-dihydro-6-methyl-3,5pyridinedicarboxylic acid 3-ethyl 5-methyl ester. A long-acting dihydropyridine calcium channel blocker. It is effective in the treatment of angina pectoris and hypertension. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH]
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Ampulla: A sac-like enlargement of a canal or duct. [NIH] Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH] Amyloidosis: A group of diseases in which protein is deposited in specific organs (localized amyloidosis) or throughout the body (systemic amyloidosis). Amyloidosis may be either primary (with no known cause) or secondary (caused by another disease, including some types of cancer). Generally, primary amyloidosis affects the nerves, skin, tongue, joints, heart, and liver; secondary amyloidosis often affects the spleen, kidneys, liver, and adrenal glands. [NIH] Anaerobic: 1. Lacking molecular oxygen. 2. Growing, living, or occurring in the absence of molecular oxygen; pertaining to an anaerobe. [EU] Anaerobic Threshold: The oxygen consumption level above which aerobic energy production is supplemented by anaerobic mechanisms during exercise, resulting in a sustained increase in lactate concentration and metabolic acidosis. The anaerobic threshold is affected by factors that modify oxygen delivery to the tissues; it is low in patients with heart disease. Methods of measurement include direct measure of lactate concentration, direct measurement of bicarbonate concentration, and gas exchange measurements. [NIH] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anaplasia: Loss of structural differentiation and useful function of neoplastic cells. [NIH] Anastomosis: A procedure to connect healthy sections of tubular structures in the body after the diseased portion has been surgically removed. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Anchorage: In dentistry, points of retention of fillings and artificial restorations and appliances. [NIH] Androgens: A class of sex hormones associated with the development and maintenance of the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anemia, Sickle Cell: A disease characterized by chronic hemolytic anemia, episodic painful
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crises, and pathologic involvement of many organs. It is the clinical expression of homozygosity for hemoglobin S. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] Anesthetics: Agents that are capable of inducing a total or partial loss of sensation, especially tactile sensation and pain. They may act to induce general anesthesia, in which an unconscious state is achieved, or may act locally to induce numbness or lack of sensation at a targeted site. [NIH] Aneurysm: A sac formed by the dilatation of the wall of an artery, a vein, or the heart. [NIH] Angina: Chest pain that originates in the heart. [NIH] Angina Pectoris: The symptom of paroxysmal pain consequent to myocardial ischemia usually of distinctive character, location and radiation, and provoked by a transient stressful situation during which the oxygen requirements of the myocardium exceed the capacity of the coronary circulation to supply it. [NIH] Anginal: Pertaining to or characteristic of angina. [EU] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Angiogenesis Factor: Substance causing proliferation of new blood vessels. It is found in tissues with high metabolic requirements, such as the retina, and in certain cancers. The factor is also released by hypoxic macrophages at the edges or outer surfaces of wounds and initiates revascularization in wound healing. [NIH] Angiogram: An x-ray of blood vessels; the person receives an injection of dye to outline the vessels on the x-ray. [NIH] Angiography: Radiography of blood vessels after injection of a contrast medium. [NIH] Angioplasty: Endovascular reconstruction of an artery, which may include the removal of atheromatous plaque and/or the endothelial lining as well as simple dilatation. These are procedures performed by catheterization. When reconstruction of an artery is performed surgically, it is called endarterectomy. [NIH] Angiotensin converting enzyme inhibitor: A drug used to decrease pressure inside blood vessels. [NIH] Angiotensin I: The decapeptide precursor of angiotensin II, generated by the action of renin on angiotensinogen. It has limited pharmacologic activity. [NIH] Angiotensin-Converting Enzyme Inhibitors: A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility. [NIH] Angiotensinogen: An alpha-globulin of which a fragment of 14 amino acids is converted by renin to angiotensin I, the inactive precursor of angiotensin II. It is a member of the serpin superfamily. [NIH] Anhydrous: Deprived or destitute of water. [EU] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers
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or other tissues are called xenograft models. [NIH] Anionic: Pertaining to or containing an anion. [EU] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Ankle: That part of the lower limb directly above the foot. [NIH] Anode: Electrode held at a positive potential with respect to a cathode. [NIH] Anomalies: Birth defects; abnormalities. [NIH] Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Antecedent: Existing or occurring before in time or order often with consequential effects. [EU]
Anterior Cerebral Artery: Artery formed by the bifurcation of the internal carotid artery. Branches of the anterior cerebral artery supply the caudate nucleus, internal capsule, putamen, septal nuclei, gyrus cinguli, and surfaces of the frontal lobe and parietal lobe. [NIH] Anterior chamber: The space in front of the iris and behind the cornea. [NIH] Anti-Arrhythmia Agents: Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade. [NIH] Antiarrhythmic: An agent that prevents or alleviates cardiac arrhythmia. [EU] Anti-Asthmatic Agents: Drugs that are used to treat asthma. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Anticholinergic: An agent that blocks the parasympathetic nerves. Called also parasympatholytic. [EU] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Anticonvulsant: An agent that prevents or relieves convulsions. [EU] Antidepressant: A drug used to treat depression. [NIH] Antidiuretic: Suppressing the rate of urine formation. [EU] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [EU]
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Antifungal: Destructive to fungi, or suppressing their reproduction or growth; effective against fungal infections. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Antihistamine: A drug that counteracts the action of histamine. The antihistamines are of two types. The conventional ones, as those used in allergies, block the H1 histamine receptors, whereas the others block the H2 receptors. Called also antihistaminic. [EU] Antihypertensive: An agent that reduces high blood pressure. [EU] Antihypertensive Agents: Drugs used in the treatment of acute or chronic hypertension regardless of pharmacological mechanism. Among the antihypertensive agents are diuretics (especially diuretics, thiazide), adrenergic beta-antagonists, adrenergic alpha-antagonists, angiotensin-converting enzyme inhibitors, calcium channel blockers, ganglionic blockers, and vasodilator agents. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU] Antimycotic: Suppressing the growth of fungi. [EU] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antineoplastic Agents: Substances that inhibit or prevent the proliferation of neoplasms. [NIH]
Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antiproliferative: Counteracting a process of proliferation. [EU] Antipruritic: Relieving or preventing itching. [EU] Antipsychotic: Effective in the treatment of psychosis. Antipsychotic drugs (called also neuroleptic drugs and major tranquilizers) are a chemically diverse (including phenothiazines, thioxanthenes, butyrophenones, dibenzoxazepines, dibenzodiazepines, and diphenylbutylpiperidines) but pharmacologically similar class of drugs used to treat schizophrenic, paranoid, schizoaffective, and other psychotic disorders; acute delirium and dementia, and manic episodes (during induction of lithium therapy); to control the movement disorders associated with Huntington's chorea, Gilles de la Tourette's syndrome, and ballismus; and to treat intractable hiccups and severe nausea and vomiting. Antipsychotic agents bind to dopamine, histamine, muscarinic cholinergic, a-adrenergic, and serotonin receptors. Blockade of dopaminergic transmission in various areas is thought to be responsible for their major effects : antipsychotic action by blockade in the mesolimbic and mesocortical areas; extrapyramidal side effects (dystonia, akathisia, parkinsonism, and
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tardive dyskinesia) by blockade in the basal ganglia; and antiemetic effects by blockade in the chemoreceptor trigger zone of the medulla. Sedation and autonomic side effects (orthostatic hypotension, blurred vision, dry mouth, nasal congestion and constipation) are caused by blockade of histamine, cholinergic, and adrenergic receptors. [EU] Antipsychotic Agents: Agents that control agitated psychotic behavior, alleviate acute psychotic states, reduce psychotic symptoms, and exert a quieting effect. They are used in schizophrenia, senile dementia, transient psychosis following surgery or myocardial infarction, etc. These drugs are often referred to as neuroleptics alluding to the tendency to produce neurological side effects, but not all antipsychotics are likely to produce such effects. Many of these drugs may also be effective against nausea, emesis, and pruritus. [NIH] Antiseptic: A substance that inhibits the growth and development of microorganisms without necessarily killing them. [EU] Antiserum: The blood serum obtained from an animal after it has been immunized with a particular antigen. It will contain antibodies which are specific for that antigen as well as antibodies specific for any other antigen with which the animal has previously been immunized. [NIH] Antithrombotic: Preventing or interfering with the formation of thrombi; an agent that so acts. [EU] Antiviral: Destroying viruses or suppressing their replication. [EU] Anuria: Inability to form or excrete urine. [NIH] Anus: The opening of the rectum to the outside of the body. [NIH] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Aortic Aneurysm: Aneurysm of the aorta. [NIH] Aortic Coarctation: Narrowing of the lumen of the aorta, caused by deformity of the aortic media. [NIH] Apnea: A transient absence of spontaneous respiration. [NIH] Apnoea: Cessation of breathing. [EU] Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid transport and metabolism. [NIH] Aponeurosis: Tendinous expansion consisting of a fibrous or membranous sheath which serves as a fascia to enclose or bind a group of muscles. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Applicability: A list of the commodities to which the candidate method can be applied as presented or with minor modifications. [NIH] Aqueous: Having to do with water. [NIH] Aqueous fluid: Clear, watery fluid that flows between and nourishes the lens and the cornea; secreted by the ciliary processes. [NIH]
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Aqueous humor: Clear, watery fluid that flows between and nourishes the lens and the cornea; secreted by the ciliary processes. [NIH] Arachidonate 15-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 15-hydroperoxyarachidonate (15-HPETE) which is rapidly converted to 15-hydroxy5,8,11,13-eicosatetraenoate (15-HETE). The 15-hydroperoxides are preferentially formed in neutrophils and lymphocytes. EC 1.13.11.33. [NIH] Arachidonate Lipoxygenases: Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates (HPETES). These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids (HETES). The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- . [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Aromatic: Having a spicy odour. [EU] Arrhythmia: Any variation from the normal rhythm or rate of the heart beat. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arteriolar: Pertaining to or resembling arterioles. [EU] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Arteriolosclerosis: Sclerosis and thickening of the walls of the smaller arteries (arterioles). Hyaline arteriolosclerosis, in which there is homogeneous pink hyaline thickening of the arteriolar walls, is associated with benign nephrosclerosis. Hyperplastic arteriolosclerosis, in which there is a concentric thickening with progressive narrowing of the lumina may be associated with malignant hypertension, nephrosclerosis, and scleroderma. [EU] Arteriosclerosis: Thickening and loss of elasticity of arterial walls. Atherosclerosis is the most common form of arteriosclerosis and involves lipid deposition and thickening of the intimal cell layers within arteries. Additional forms of arteriosclerosis involve calcification of the media of muscular arteries (Monkeberg medial calcific sclerosis) and thickening of the walls of small arteries or arterioles due to cell proliferation or hyaline deposition (arteriolosclerosis). [NIH] Arteriosus: Circle composed of anastomosing arteries derived from two long posterior ciliary and seven anterior ciliary arteries, located in the ciliary body about the root of the iris. [NIH]
Arteriovenous: Both arterial and venous; pertaining to or affecting an artery and a vein. [EU] Arteriovenous Fistula: An abnormal communication between an artery and a vein. [NIH] Arteritis: Inflammation of an artery. [NIH] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Articular: Of or pertaining to a joint. [EU] Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is
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considered an antioxidant. [NIH] Aseptic: Free from infection or septic material; sterile. [EU] Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Asthenia: Clinical sign or symptom manifested as debility, or lack or loss of strength and energy. [NIH] Astringents: Agents, usually topical, that cause the contraction of tissues for the control of bleeding or secretions. [NIH] Astrocytes: The largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the blood brain barrier. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with microglia) respond to injury. Astrocytes have high- affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitter, but their role in signaling (as in many other functions) is not well understood. [NIH] Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atenolol: A cardioselective beta-adrenergic blocker possessing properties and potency similar to propranolol, but without a negative inotropic effect. [NIH] Atopic: Pertaining to an atopen or to atopy; allergic. [EU] Atresia: Lack of a normal opening from the esophagus, intestines, or anus. [NIH] Atrial: Pertaining to an atrium. [EU] Atrial Fibrillation: Disorder of cardiac rhythm characterized by rapid, irregular atrial impulses and ineffective atrial contractions. [NIH] Atrial Natriuretic Factor: A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight peptides derived from a common precursor and secreted by the heart atria. All these peptides share a sequence of about 20 amino acids. [NIH] Atrioventricular: Pertaining to an atrium of the heart and to a ventricle. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuation: Reduction of transmitted sound energy or its electrical equivalent. [NIH] Auditory: Pertaining to the sense of hearing. [EU]
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Autacoids: A chemically diverse group of substances produced by various tissues in the body that cause slow contraction of smooth muscle; they have other intense but varied pharmacologic activities. [NIH] Autodigestion: Autolysis; a condition found in disease of the stomach: the stomach wall is digested by the gastric juice. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Autonomic Neuropathy: A disease of the nerves affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a person's conscious control and function automatically. Also called visceral neuropathy. [NIH] Autoradiography: A process in which radioactive material within an object produces an image when it is in close proximity to a radiation sensitive emulsion. [NIH] Avian: A plasmodial infection in birds. [NIH] Axillary: Pertaining to the armpit area, including the lymph nodes that are located there. [NIH]
Axillary Artery: The continuation of the subclavian artery; it distributes over the upper limb, axilla, chest and shoulder. [NIH] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body. [NIH] Azotemia: An excess of urea or other nitrogenous compounds in the blood. [EU] Backcross: A cross between a hybrid and either one of its parents. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bactericide: An agent that destroys bacteria. [EU] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacteriuria: The presence of bacteria in the urine with or without consequent urinary tract infection. Since bacteriuria is a clinical entity, the term does not preclude the use of urine/microbiology for technical discussions on the isolation and segregation of bacteria in the urine. [NIH] Barbiturate: A drug with sedative and hypnotic effects. Barbiturates have been used as sedatives and anesthetics, and they have been used to treat the convulsions associated with
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epilepsy. [NIH] Baroreflex: A negative feedback system which buffers short-term changes in blood pressure. Increased pressure stretches blood vessels which activates pressoreceptors (baroreceptors) in the vessel walls. The net response of the central nervous system is a reduction of central sympathetic outflow. This reduces blood pressure both by decreasing peripheral vascular resistance and by lowering cardiac output. Because the baroreceptors are tonically active, the baroreflex can compensate rapidly for both increases and decreases in blood pressure. [NIH]
Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Basilar Artery: The artery formed by the union of the right and left vertebral arteries; it runs from the lower to the upper border of the pons, where it bifurcates into the two posterior cerebral arteries. [NIH] Basophil: A type of white blood cell. Basophils are granulocytes. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Bereavement: Refers to the whole process of grieving and mourning and is associated with a deep sense of loss and sadness. [NIH] Beta blocker: A drug used to slow the heart rate and reduce pressure inside blood vessels. It also can regulate heart rhythm. [NIH] Beta-Thalassemia: A disorder characterized by reduced synthesis of the beta chains of hemoglobin. There is retardation of hemoglobin A synthesis in the heterozygous form (thalassemia minor), which is asymptomatic, while in the homozygous form (thalassemia major, Cooley's anemia, Mediterranean anemia, erythroblastic anemia), which can result in severe complications and even death, hemoglobin A synthesis is absent. [NIH] Betaxolol: A cardioselective beta-1-adrenergic antagonist with no partial agonist activity. [NIH]
Bifida: A defect in development of the vertebral column in which there is a central deficiency of the vertebral lamina. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH]
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Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile duct: A tube through which bile passes in and out of the liver. [NIH] Bile Pigments: Pigments that give a characteristic color to bile including: bilirubin, biliverdine, and bilicyanin. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Biliary Tract: The gallbladder and its ducts. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biometry: The use of statistical methods to analyze biological observations and phenomena. [NIH]
Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Birth Injuries: Mechanical or anoxic trauma incurred by the infant during labor or delivery. [NIH]
Bladder: The organ that stores urine. [NIH] Blastocyst: The mammalian embryo in the post-morula stage in which a fluid-filled cavity, enclosed primarily by trophoblast, contains an inner cell mass which becomes the embryonic disc. [NIH] Blinking: Brief closing of the eyelids by involuntary normal periodic closing, as a protective measure, or by voluntary action. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Flow Velocity: A value equal to the total volume flow divided by the cross-sectional
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area of the vascular bed. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood transfusion: The administration of blood or blood products into a blood vessel. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood Viscosity: The internal resistance of the blood to shear forces. The in vitro measure of whole blood viscosity is of limited clinical utility because it bears little relationship to the actual viscosity within the circulation, but an increase in the viscosity of circulating blood can contribute to morbidity in patients suffering from disorders such as sickle cell anemia and polycythemia. [NIH] Blood Volume: Volume of circulating blood. It is the sum of the plasma volume and erythrocyte volume. [NIH] Blood-Brain Barrier: Specialized non-fenestrated tightly-joined endothelial cells (tight junctions) that form a transport barrier for certain substances between the cerebral capillaries and the brain tissue. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]
Body Composition: The relative amounts of various components in the body, such as percent body fat. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Body Image: Individuals' personal concept of their bodies as objects in and bound by space, independently and apart from all other objects. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH] Body Regions: Anatomical areas of the body. [NIH] Bombesin: A tetradecapeptide originally obtained from the skins of toads Bombina bombina and B. variegata. It is also an endogenous neurotransmitter in many animals including mammals. Bombesin affects vascular and other smooth muscle, gastric secretion, and renal circulation and function. [NIH] Bone Density: The amount of mineral per square centimeter of bone. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by photon absorptiometry or x-ray computed tomography. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone scan: A technique to create images of bones on a computer screen or on film. A small amount of radioactive material is injected into a blood vessel and travels through the
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bloodstream; it collects in the bones and is detected by a scanner. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Brachial: All the nerves from the arm are ripped from the spinal cord. [NIH] Brachial Artery: The continuation of the axillary artery; it branches into the radial and ulnar arteries. [NIH] Brachiocephalic Veins: Large veins on either side of the root of the neck formed by the junction of the internal jugular and subclavian veins. They drain blood from the head, neck, and upper extremities, and unite to form the superior vena cava. [NIH] Bradycardia: Excessive slowness in the action of the heart, usually with a heart rate below 60 beats per minute. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Brain Ischemia: Localized reduction of blood flow to brain tissue due to arterial obtruction or systemic hypoperfusion. This frequently occurs in conjuction with brain hypoxia. Prolonged ischemia is associated with brain infarction. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]
Breakdown: A physical, metal, or nervous collapse. [NIH] Breeding: The science or art of changing the constitution of a population of plants or animals through sexual reproduction. [NIH] Bromine: A halogen with the atomic symbol Br, atomic number 36, and atomic weight 79.904. It is a volatile reddish-brown liquid that gives off suffocating vapors, is corrosive to the skin, and may cause severe gastroenteritis if ingested. [NIH] Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Bronchiectasis: Persistent abnormal dilatation of the bronchi. [NIH] Bronchioles: The tiny branches of air tubes in the lungs. [NIH] Bronchiolitis: Inflammation of the bronchioles. [NIH] Bronchiseptica: A small, gram-negative, motile bacillus. A normal inhabitant of the respiratory tract in man, dogs, and pigs, but is also associated with canine infectious tracheobronchitis and atrophic rhinitis in pigs. [NIH] Bronchitis: Inflammation (swelling and reddening) of the bronchi. [NIH] Bronchodilator: A drug that relaxes the smooth muscles in the constricted airway. [NIH] Bronchopulmonary: Pertaining to the lungs and their air passages; both bronchial and pulmonary. [EU] Bronchopulmonary Dysplasia: A chronic lung disease appearing in certain newborn infants
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treated for respiratory distress syndrome with mechanical ventilation and elevated concentration of inspired oxygen. [NIH] Bronchoscopy: Endoscopic examination, therapy or surgery of the bronchi. [NIH] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Buffers: A chemical system that functions to control the levels of specific ions in solution. When the level of hydrogen ion in solution is controlled the system is called a pH buffer. [NIH]
Bumetanide: A sulfamyl diuretic. [NIH] Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [NIH] Cadmium: An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to cadmium poisoning. [NIH] Cadmium Poisoning: Poisoning occurring after exposure to cadmium compounds or fumes. It may cause gastrointestinal syndromes, anemia, or pneumonitis. [NIH] Calcification: Deposits of calcium in the tissues of the breast. Calcification in the breast can be seen on a mammogram, but cannot be detected by touch. There are two types of breast calcification, macrocalcification and microcalcification. Macrocalcifications are large deposits and are usually not related to cancer. Microcalcifications are specks of calcium that may be found in an area of rapidly dividing cells. Many microcalcifications clustered together may be a sign of cancer. [NIH] Calcineurin: A calcium- and calmodulin-binding protein present in highest concentrations in the central nervous system. Calcineurin is composed of two subunits. A catalytic subunit, calcineurin A, and a regulatory subunit, calcineurin B, with molecular weights of about 60 kD and 19 kD, respectively. Calcineurin has been shown to dephosphorylate a number of phosphoproteins including histones, myosin light chain, and the regulatory subunit of cAMP-dependent protein kinase. It is involved in the regulation of signal transduction and is the target of an important class of immunophilin-immunosuppressive drug complexes in T-lymphocytes that act by inhibiting T-cell activation. EC 3.1.3.-. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium channel blocker: A drug used to relax the blood vessel and heart muscle, causing pressure inside blood vessels to drop. It also can regulate heart rhythm. [NIH] Calcium Channel Blockers: A class of drugs that act by selective inhibition of calcium influx through cell membranes or on the release and binding of calcium in intracellular pools. Since they are inducers of vascular and other smooth muscle relaxation, they are used in the drug therapy of hypertension and cerebrovascular spasms, as myocardial protective agents, and in the relaxation of uterine spasms. [NIH] Calcium Channels: Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue. [NIH]
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Calcium Oxalate: The calcium salt of oxalic acid, occurring in the urine as crystals and in certain calculi. [NIH] Calculi: An abnormal concretion occurring mostly in the urinary and biliary tracts, usually composed of mineral salts. Also called stones. [NIH] Callus: A callosity or hard, thick skin; the bone-like reparative substance that is formed round the edges and fragments of broken bone. [NIH] Calmodulin: A heat-stable, low-molecular-weight activator protein found mainly in the brain and heart. The binding of calcium ions to this protein allows this protein to bind to cyclic nucleotide phosphodiesterases and to adenyl cyclase with subsequent activation. Thereby this protein modulates cyclic AMP and cyclic GMP levels. [NIH] Calsequestrin: Acidic protein found in sarcoplasmic reticulum that binds calcium to the extent of 700-900 nmoles/mg. It plays the role of sequestering calcium transported to the interior of the intracellular vesicle. [NIH] Camphor: A bicyclic monoterpene ketone found widely in plant (primarily the camphor tree, Cinnamomum camphora). Natural camphor is used topically as a skin antipruritic and as an anti-infective agent. [NIH] Cannabidiol: Compound isolated from Cannabis sativa extract. [NIH] Cannabinoids: Compounds extracted from Cannabis sativa L. and metabolites having the cannabinoid structure. The most active constituents are tetrahydrocannabinol, cannabinol, and cannabidiol. [NIH] Cannabinol: A physiologically inactive constituent of Cannabis sativa L. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capillary Permeability: Property of blood capillary walls that allows for the selective exchange of substances. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (tight junctions) which may limit large molecule movement. [NIH] Capsaicin: Cytotoxic alkaloid from various species of Capsicum (pepper, paprika), of the Solanaceae. [NIH] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Captopril: A potent and specific inhibitor of peptidyl-dipeptidase A. It blocks the conversion of angiotensin I to angiotensin II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the renin-angiotensin system and inhibits pressure responses to exogenous angiotensin. [NIH] Carbachol: A slowly hydrolyzed cholinergic agonist that acts at both muscarinic and nicotinic receptors. [NIH] Carbamazepine: An anticonvulsant used to control grand mal and psychomotor or focal seizures. Its mode of action is not fully understood, but some of its actions resemble those of phenytoin; although there is little chemical resemblance between the two compounds, their three-dimensional structure is similar. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates
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are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carbonate Dehydratase: A zinc-containing enzyme of erythrocytes with molecular weight of 30 kD. It is among the most active of known enzymes and catalyzes the reversible hydration of carbon dioxide, which is significant in the transport of CO2 from the tissues to the lungs. The enzyme is inhibited by acetazolamide. EC 4.2.1.1. [NIH] Carbonic Anhydrase Inhibitors: A class of compounds that reduces the secretion of H+ ions by the proximal kidney tubule through inhibition of carbonic anhydrase (carbonate dehydratase). [NIH] Carboxy: Cannabinoid. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinogens: Substances that increase the risk of neoplasms in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. [NIH] Cardenolides: C(23)-steroids with methyl groups at C-10 and C-13 and a five-membered lactone at C-17. They are aglycone constituents of cardiac glycosides and must have at least one double bond in the molecule. the class includes cardadienolides and cardatrienolides. Members include digitoxin and digoxin and their derivatives and the strophanthins. [NIH] Cardiac: Having to do with the heart. [NIH] Cardiac Glycosides: Substances obtained from species of Digitalis, Strophanthus, and other plants that contain specific steroid glycosides or their semisynthetic derivatives and used in congestive heart failure. They increase the force of cardiac contraction without significantly affecting other parameters, but are very toxic at larger doses. Their mechanism of action usually involves inhibition of the Na(+)-K(+)-exchanging ATPase and they are often used in cell biological studies for that purpose. [NIH] Cardiac Output: The volume of blood passing through the heart per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with stroke volume (volume per beat). [NIH] Cardiogenic: Originating in the heart; caused by abnormal function of the heart. [EU] Cardiology: The study of the heart, its physiology, and its functions. [NIH] Cardiomyopathy: A general diagnostic term designating primary myocardial disease, often of obscure or unknown etiology. [EU] Cardiopulmonary: Having to do with the heart and lungs. [NIH] Cardiopulmonary Bypass: Diversion of the flow of blood from the entrance of the right atrium directly to the aorta (or femoral artery) via an oxygenator thus bypassing both the heart and lungs. [NIH] Cardiorespiratory: Relating to the heart and lungs and their function. [EU] Cardioselective: Having greater activity on heart tissue than on other tissue. [EU] Cardiotonic: 1. Having a tonic effect on the heart. 2. An agent that has a tonic effect on the heart. [EU] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular Agents: Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume. [NIH]
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Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Cardiovascular Physiology: Functions and activities of the cardiovascular system as a whole or of any of its parts. [NIH] Cardiovascular System: The heart and the blood vessels by which blood is pumped and circulated through the body. [NIH] Carnitine: Constituent of striated muscle and liver. It is used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias. [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Carotid Arteries: Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery. [NIH] Carotid Body: A small cluster of chemoreceptive and supporting cells located near the bifurcation of the internal carotid artery. The carotid body, which is richly supplied with fenestrated capillaries, senses the pH, carbon dioxide, and oxygen concentrations in the blood and plays a crucial role in their homeostatic control. [NIH] Carotid Sinus: The dilated portion of the common carotid artery at its bifurcation into external and internal carotids. It contains baroreceptors which, when stimulated, cause slowing of the heart, vasodilatation, and a fall in blood pressure. [NIH] Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Catabolism: Any destructive metabolic process by which organisms convert substances into excreted compounds. [EU] Catalase: An oxidoreductase that catalyzes the conversion of hydrogen peroxide to water and oxygen. It is present in many animal cells. A deficiency of this enzyme results in acatalasia. EC 1.11.1.6. [NIH] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [NIH] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in obstructions. [NIH]
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Cathode: An electrode, usually an incandescent filament of tungsten, which emits electrons in an X-ray tube. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] Causal: Pertaining to a cause; directed against a cause. [EU] Causality: The relating of causes to the effects they produce. Causes are termed necessary when they must always precede an effect and sufficient when they initiate or produce an effect. Any of several factors may be associated with the potential disease causation or outcome, including predisposing factors, enabling factors, precipitating factors, reinforcing factors, and risk factors. [NIH] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Caveolae: Endocytic/exocytic cell membrane structures rich in glycosphingolipids, cholesterol, and lipid-anchored membrane proteins that function in endocytosis (potocytosis), transcytosis, and signal transduction. Caveolae assume various shapes from open pits to closed vesicles. Caveolar coats are composed of caveolins. [NIH] Caveolins: The main structural proteins of caveolae. Several distinct genes for caveolins have been identified. [NIH] Celecoxib: A drug that reduces pain. Celecoxib belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is being studied for cancer prevention. [NIH] Celiac Artery: The arterial trunk that arises from the abdominal aorta and after a short course divides into the left gastric, common hepatic and splenic arteries. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH] Cell Adhesion Molecules: Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell Membrane Structures: Structures which are part of the cell membrane or have cell membrane as a major part of their structure. [NIH] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which
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oxygen is used to provide a source of energy for the cell. [NIH] Cell Size: The physical dimensions of a cell. It refers mainly to changes in dimensions correlated with physiological or pathological changes in cells. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Central Nervous System Infections: Pathogenic infections of the brain, spinal cord, and meninges. DNA virus infections; RNA virus infections; bacterial infections; mycoplasma infections; Spirochaetales infections; fungal infections; protozoan infections; helminthiasis; and prion diseases may involve the central nervous system as a primary or secondary process. [NIH] Centrifugation: A method of separating organelles or large molecules that relies upon differential sedimentation through a preformed density gradient under the influence of a gravitational field generated in a centrifuge. [NIH] Ceramide: A type of fat produced in the body. It may cause some types of cells to die, and is being studied in cancer treatment. [NIH] Cerebellar: Pertaining to the cerebellum. [EU] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral Angiography: Radiography of the vascular system of the brain after injection of a contrast medium. [NIH] Cerebral Arteries: The arteries supplying the cerebral cortex. [NIH] Cerebral Cortex: The thin layer of gray matter on the surface of the cerebral hemisphere that develops from the telencephalon and folds into gyri. It reaches its highest development in man and is responsible for intellectual faculties and higher mental functions. [NIH] Cerebral hemispheres: The two halves of the cerebrum, the part of the brain that controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. The right hemisphere controls muscle movement on the left side of the body, and the left hemisphere controls muscle movement on the right side of the body. [NIH] Cerebral Hemorrhage: Bleeding into a cerebral hemisphere of the brain, including lobar, subcortical white matter, and basal ganglia hemorrhages. Commonly associated conditions include hypertension; intracranial arteriosclerosis; intracranial aneurysm; craniocerebral trauma; intracranial arteriovenous malformations; cerebral amyloid angiopathy; and cerebral infarction. [NIH] Cerebral Infarction: The formation of an area of necrosis in the cerebrum caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., infarction, anterior cerebral artery), and etiology (e.g., embolic infarction). [NIH]
Cerebral Palsy: Refers to a motor disability caused by a brain dysfunction. [NIH] Cerebral Veins: Veins draining the cerebrum. [NIH]
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Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrospinal Fluid Pressure: Manometric pressure of the cerebrospinal fluid as measured by lumbar, cerebroventricular, or cisternal puncture. Within the cranial cavity it is called intracranial pressure. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chemoreceptor: A receptor adapted for excitation by chemical substances, e.g., olfactory and gustatory receptors, or a sense organ, as the carotid body or the aortic (supracardial) bodies, which is sensitive to chemical changes in the blood stream, especially reduced oxygen content, and reflexly increases both respiration and blood pressure. [EU] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotherapeutic agent: A drug used to treat cancer. [NIH] Chenodeoxycholic Acid: A bile acid, usually conjugated with either glycine or taurine. It acts as a detergent to solubilize fats for intestinal absorption and is reabsorbed by the small intestine. It is used as cholagogue, a choleretic laxative, and to prevent or dissolve gallstones. [NIH] Chest Pain: Pressure, burning, or numbness in the chest. [NIH] Chest wall: The ribs and muscles, bones, and joints that make up the area of the body between the neck and the abdomen. [NIH] Chin: The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for the passage of blood vessels and a nerve. [NIH] Chiropractic: A system of treating bodily disorders by manipulation of the spine and other parts, based on the belief that the cause is the abnormal functioning of a nerve. [NIH] Chlorine: A greenish-yellow, diatomic gas that is a member of the halogen family of elements. It has the atomic symbol Cl, atomic number 17, and atomic weight 70.906. It is a powerful irritant that can cause fatal pulmonary edema. Chlorine is used in manufacturing, as a reagent in synthetic chemistry, for water purification, and in the production of chlorinated lime, which is used in fabric bleaching. [NIH] Chlorogenic Acid: A naturally occuring phenolic acid which is a carcinogenic inhibitor. It
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has also been shown to prevent paraquat-induced oxidative stress in rats. (From J Chromatogr A 1996;741(2):223-31; Biosci Biotechnol Biochem 1996;60(5):765-68). [NIH] Choleretic: A choleretic agent. [EU] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Choroid: The thin, highly vascular membrane covering most of the posterior of the eye between the retina and sclera. [NIH] Choroid Plexus: A villous structure of tangled masses of blood vessels contained within the third, lateral, and fourth ventricles of the brain. It regulates part of the production and composition of cerebrospinal fluid. [NIH] Chromaffin System: The cells of the body which stain with chromium salts. They occur along the sympathetic nerves, in the adrenal gland, and in various other organs. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic Obstructive Pulmonary Disease: Collective term for chronic bronchitis and emphysema. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from the small intestines to the tissues. [NIH] Chymopapain: A cysteine endopeptidase isolated from papaya latex. Preferential cleavage at glutamic and aspartic acid residues. EC 3.4.22.6. [NIH] Ciliary: Inflammation or infection of the glands of the margins of the eyelids. [NIH] Ciliary Arteries: Three groups of arteries found in the eye which supply the iris, pupil, sclera, conjunctiva, and the muscles of the iris. [NIH] Ciliary Body: A ring of tissue extending from the scleral spur to the ora serrata of the retina. It consists of the uveal portion and the epithelial portion. The ciliary muscle is in the uveal portion and the ciliary processes are in the epithelial portion. [NIH] Ciliary processes: The extensions or projections of the ciliary body that secrete aqueous humor. [NIH] Cinnarizine: A piperazine derivative with histamine H1-receptor and calcium-channel blocking activity and considerable antiemetic properties. [NIH] Circadian: Repeated more or less daily, i. e. on a 23- to 25-hour cycle. [NIH]
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Circadian Rhythm: The regular recurrence, in cycles of about 24 hours, of biological processes or activities, such as sensitivity to drugs and stimuli, hormone secretion, sleeping, feeding, etc. This rhythm seems to be set by a 'biological clock' which seems to be set by recurring daylight and darkness. [NIH] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] Cirrhosis: A type of chronic, progressive liver disease. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Citric Acid: A key intermediate in metabolism. It is an acid compound found in citrus fruits. The salts of citric acid (citrates) can be used as anticoagulants due to their calcium chelating ability. [NIH] Citrus: Any tree or shrub of the Rue family or the fruit of these plants. [NIH] Clamp: A u-shaped steel rod used with a pin or wire for skeletal traction in the treatment of certain fractures. [NIH] Clear cell carcinoma: A rare type of tumor of the female genital tract in which the inside of the cells looks clear when viewed under a microscope. [NIH] Cleave: A double-stranded cut in DNA with a restriction endonuclease. [NIH] Climacteric: Physiologic period, characterized by endocrine, somatic, and psychic changes with the termination of ovarian function in the female. It may also accompany the normal diminution of sexual activity in the male. [NIH] Clindamycin: An antibacterial agent that is a semisynthetic analog of lincomycin. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]
Clinical Protocols: Precise and detailed plans for the study of a medical or biomedical problem and/or plans for a regimen of therapy. [NIH] Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Cloprostenol: A synthetic prostaglandin F2alpha analog. The compound has luteolytic effects and is used for the synchronization of estrus in cattle. [NIH] Clot Retraction: Retraction of a clot resulting from contraction of platelet pseudopods attached to fibrin strands that is dependent on the contractile protein thrombosthenin. Used as a measure of platelet function. [NIH] Clotrimazole: An imidazole derivative with a broad spectrum of antimycotic activity. It inhibits biosynthesis of the sterol ergostol, an important component of fungal cell
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membranes. Its action leads to increased membrane permeability and apparent disruption of enzyme systems bound to the membrane. [NIH] Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which causes the separation of the system into a liquid phase and an insoluble mass called the clot or curd. Coagulation is usually irreversible. 3. In surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation. [EU] Coal: A natural fuel formed by partial decomposition of vegetable matter under certain environmental conditions. [NIH] Coal Tar: A by-product of the destructive distillation of coal used as a topical antieczematic. It is an antipruritic and keratoplastic agent used also in the treatment of psoriasis and other skin conditions. Occupational exposure to soots, tars, and certain mineral oils is known to be carcinogenic according to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985) (Merck Index, 11th ed). [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cognition: Intellectual or mental process whereby an organism becomes aware of or obtains knowledge. [NIH] Cognitive restructuring: A method of identifying and replacing fear-promoting, irrational beliefs with more realistic and functional ones. [NIH] Cohort Studies: Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics. [NIH] Colic: Paroxysms of pain. This condition usually occurs in the abdominal region but may occur in other body regions as well. [NIH] Colitis: Inflammation of the colon. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collagen disease: A term previously used to describe chronic diseases of the connective tissue (e.g., rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis), but now is thought to be more appropriate for diseases associated with defects in collagen, which is a component of the connective tissue. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colloidal: Of the nature of a colloid. [EU] Colon: The long, coiled, tubelike organ that removes water from digested food. The
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remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Colorectal: Having to do with the colon or the rectum. [NIH] Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [NIH] Comorbidity: The presence of co-existing or additional diseases with reference to an initial diagnosis or with reference to the index condition that is the subject of study. Comorbidity may affect the ability of affected individuals to function and also their survival; it may be used as a prognostic indicator for length of hospital stay, cost factors, and outcome or survival. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complete remission: The disappearance of all signs of cancer. Also called a complete response. [NIH] Compliance: Distensibility measure of a chamber such as the lungs (lung compliance) or bladder. Compliance is expressed as a change in volume per unit change in pressure. [NIH] Compress: A plug used to occludate an orifice in the control of bleeding, or to mop up secretions; an absorbent pad. [NIH]
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Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized axial tomography (CAT) scan and computed tomography (CT scan). [NIH] Concentric: Having a common center of curvature or symmetry. [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU] Conduction: The transfer of sound waves, heat, nervous impulses, or electricity. [EU] Cones: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide sharp central vision and color vision. [NIH] Confounding: Extraneous variables resulting in outcome effects that obscure or exaggerate the "true" effect of an intervention. [NIH] Congestive heart failure: Weakness of the heart muscle that leads to a buildup of fluid in body tissues. [NIH] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue Cells: A group of cells that includes fibroblasts, cartilage cells, adipocytes, smooth muscle cells, and bone cells. [NIH] Connective Tissue Diseases: A heterogeneous group of disorders, some hereditary, others acquired, characterized by abnormal structure or function of one or more of the elements of connective tissue, i.e., collagen, elastin, or the mucopolysaccharides. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Constrict: Tighten; narrow. [NIH] Constriction: The act of constricting. [NIH] Constriction, Pathologic: The condition of an anatomical structure's being constricted beyond normal dimensions. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Contamination: The soiling or pollution by inferior material, as by the introduction of organisms into a wound, or sewage into a stream. [EU]
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Continuous infusion: The administration of a fluid into a blood vessel, usually over a prolonged period of time. [NIH] Contractility: Capacity for becoming short in response to a suitable stimulus. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Contralateral: Having to do with the opposite side of the body. [NIH] Contrast Media: Substances used in radiography that allow visualization of certain tissues. [NIH]
Contrast medium: A substance that is introduced into or around a structure and, because of the difference in absorption of x-rays by the contrast medium and the surrounding tissues, allows radiographic visualization of the structure. [EU] Controlled clinical trial: A clinical study that includes a comparison (control) group. The comparison group receives a placebo, another treatment, or no treatment at all. [NIH] Controlled study: An experiment or clinical trial that includes a comparison (control) group. [NIH]
Conus: A large, circular, white patch around the optic disk due to the exposing of the sclera as a result of degenerative change or congenital abnormality in the choroid and retina. [NIH] Convulsions: A general term referring to sudden and often violent motor activity of cerebral or brainstem origin. Convulsions may also occur in the absence of an electrical cerebral discharge (e.g., in response to hypotension). [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Cor: The muscular organ that maintains the circulation of the blood. c. adiposum a heart that has undergone fatty degeneration or that has an accumulation of fat around it; called also fat or fatty, heart. c. arteriosum the left side of the heart, so called because it contains oxygenated (arterial) blood. c. biloculare a congenital anomaly characterized by failure of formation of the atrial and ventricular septums, the heart having only two chambers, a single atrium and a single ventricle, and a common atrioventricular valve. c. bovinum (L. 'ox heart') a greatly enlarged heart due to a hypertrophied left ventricle; called also c. taurinum and bucardia. c. dextrum (L. 'right heart') the right atrium and ventricle. c. hirsutum, c. villosum. c. mobile (obs.) an abnormally movable heart. c. pendulum a heart so movable that it seems to be hanging by the great blood vessels. c. pseudotriloculare biatriatum a congenital cardiac anomaly in which the heart functions as a three-chambered heart because of tricuspid atresia, the right ventricle being extremely small or rudimentary and the right atrium greatly dilated. Blood passes from the right to the left atrium and thence disease due to pulmonary hypertension secondary to disease of the lung, or its blood vessels, with hypertrophy of the right ventricle. [EU] Cor pulmonale: Heart disease that results from resistance to the passage of blood through the lungs; it often leads to right heart failure. [NIH] Cornea: The transparent part of the eye that covers the iris and the pupil and allows light to enter the inside. [NIH] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary Arteriosclerosis: Thickening and loss of elasticity of the coronary arteries. [NIH] Coronary Artery Bypass: Surgical therapy of ischemic coronary artery disease achieved by grafting a section of saphenous vein, internal mammary artery, or other substitute between
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the aorta and the obstructed coronary artery distal to the obstructive lesion. [NIH] Coronary Circulation: The circulation of blood through the coronary vessels of the heart. [NIH]
Coronary Disease: Disorder of cardiac function due to an imbalance between myocardial function and the capacity of the coronary vessels to supply sufficient flow for normal function. It is a form of myocardial ischemia (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels. [NIH] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Coronary Vasospasm: Spasm of the large- or medium-sized coronary arteries. [NIH] Coronary Vessels: The veins and arteries of the heart. [NIH] Corpus: The body of the uterus. [NIH] Corpus Luteum: The yellow glandular mass formed in the ovary by an ovarian follicle that has ruptured and discharged its ovum. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to angiotensin II. They are divided, according to their predominant biological activity, into three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cost Savings: Reductions in all or any portion of the costs of providing goods or services. Savings may be incurred by the provider or the consumer. [NIH] Cost-benefit: A quantitative technique of economic analysis which, when applied to radiation practice, compares the health detriment from the radiation doses concerned with the cost of radiation dose reduction in that practice. [NIH] Cost-Benefit Analysis: A method of comparing the cost of a program with its expected benefits in dollars (or other currency). The benefit-to-cost ratio is a measure of total return expected per unit of money spent. This analysis generally excludes consideration of factors that are not measured ultimately in economic terms. Cost effectiveness compares alternative ways to achieve a specific set of results. [NIH]
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Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Craniotomy: An operation in which an opening is made in the skull. [NIH] Creatinine: A compound that is excreted from the body in urine. Creatinine levels are measured to monitor kidney function. [NIH] Creatinine clearance: A test that measures how efficiently the kidneys remove creatinine and other wastes from the blood. Low creatinine clearance indicates impaired kidney function. [NIH] Criterion: A standard by which something may be judged. [EU] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Cross-Sectional Studies: Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with longitudinal studies which are followed over a period of time. [NIH] Crystalluria: The excretion of crystals in the urine, producing renal irritation. [EU] Cultured cells: Animal or human cells that are grown in the laboratory. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH] Cyanosis: A bluish or purplish discoloration of the skin and mucous membranes due to an increase in the amount of deoxygenated hemoglobin in the blood or a structural defect in the hemoglobin molecule. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclin: Molecule that regulates the cell cycle. [NIH] Cyclodextrins: A homologous group of cyclic glucans consisting of alpha-1,4 bound glucose units obtained by the action of cyclodextrin glucanotransferase on starch or similar substrates. The enzyme is produced by certain species of Bacillus. Cyclodextrins form inclusion complexes with a wide variety of substances. [NIH] Cyclooxygenase Inhibitors: Compounds or agents that combine with cyclooxygenase (prostaglandin-endoperoxide synthase) and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of eicosanoids, prostaglandins, and thromboxanes. [NIH] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH] Cyproheptadine: A serotonin antagonist and a histamine H1 blocker used as antipruritic, appetite stimulant, antiallergic, and for the post-gastrectomy dumping syndrome, etc. [NIH] Cyst: A sac or capsule filled with fluid. [NIH] Cystathionine beta-Synthase: A multifunctional pyridoxal phosphate enzyme. In the second stage of cysteine biosynthesis it catalyzes the reaction of homocysteine with serine to
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form cystathionine with the elimination of water. Deficiency of this enzyme leads to hyperhomocysteinemia and homocystinuria. EC 4.2.1.22. [NIH] Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytogenetics: A branch of genetics which deals with the cytological and molecular behavior of genes and chromosomes during cell division. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] Dairy Products: Raw and processed or manufactured milk and milk-derived products. These are usually from cows (bovine) but are also from goats, sheep, reindeer, and water buffalo. [NIH] Day Care: Institutional health care of patients during the day. The patients return home at night. [NIH] Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide, from a chemical compound. [NIH] Decidua: The epithelial lining of the endometrium that is formed before the fertilized ovum reaches the uterus. The fertilized ovum embeds in the decidua. If the ovum is not fertilized, the decidua is shed during menstruation. [NIH] Decision Making: The process of making a selective intellectual judgment when presented with several complex alternatives consisting of several variables, and usually defining a course of action or an idea. [NIH] Decompensation: Failure of compensation; cardiac decompensation is marked by dyspnea, venous engorgement, and edema. [EU] Decompression: Decompression external to the body, most often the slow lessening of external pressure on the whole body (especially in caisson workers, deep sea divers, and persons who ascend to great heights) to prevent decompression sickness. It includes also sudden accidental decompression, but not surgical (local) decompression or decompression applied through body openings. [NIH]
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Decongestant: An agent that reduces congestion or swelling. [EU] Defense Mechanisms: Unconscious process used by an individual or a group of individuals in order to cope with impulses, feelings or ideas which are not acceptable at their conscious level; various types include reaction formation, projection and self reversal. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Dehydration: The condition that results from excessive loss of body water. [NIH] Deja Vu: A subjective feeling that an experience which is occurring for the first time has been experienced before. [NIH] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delivery of Health Care: The concept concerned with all aspects of providing and distributing health services to a patient population. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dental Caries: Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp. The three most prominent theories used to explain the etiology of the disase are that acids produced by bacteria lead to decalcification; that micro-organisms destroy the enamel protein; or that keratolytic micro-organisms produce chelates that lead to decalcification. [NIH]
Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Depressive Disorder: An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent. [NIH] Deprivation: Loss or absence of parts, organs, powers, or things that are needed. [EU] Dermatitis: Any inflammation of the skin. [NIH] DES: Diethylstilbestrol. A synthetic hormone that was prescribed from the early 1940s until 1971 to help women with complications of pregnancy. DES has been linked to an increased risk of clear cell carcinoma of the vagina in daughters of women who used DES. DES may also increase the risk of breast cancer in women who used DES. [NIH] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and immunotherapy. [EU] Detergents: Purifying or cleansing agents, usually salts of long-chain aliphatic bases or acids, that exert cleansing (oil-dissolving) and antimicrobial effects through a surface action
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that depends on possessing both hydrophilic and hydrophobic properties. [NIH] Detoxification: Treatment designed to free an addict from his drug habit. [EU] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Deuterium Oxide: The isotopic compound of hydrogen of mass 2 (deuterium) with oxygen. (From Grant & Hackh's Chemical Dictionary, 5th ed) It is used to study mechanisms and rates of chemical or nuclear reactions, as well as biological processes. [NIH] Developed Countries: Countries that have reached a level of economic achievement through an increase of production, per capita income and consumption, and utilization of natural and human resources. [NIH] Dexamethasone: (11 beta,16 alpha)-9-Fluoro-11,17,21-trihydroxy-16-methylpregna-1,4diene-3,20-dione. An anti-inflammatory glucocorticoid used either in the free alcohol or esterified form in treatment of conditions that respond generally to cortisone. [NIH] Dextrorotatory: Turning towards the right hand. [NIH] Diabetes Insipidus: A metabolic disorder due to disorders in the production or release of vasopressin. It is characterized by the chronic excretion of large amounts of low specific gravity urine and great thirst. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diabetic Retinopathy: Retinopathy associated with diabetes mellitus, which may be of the background type, progressively characterized by microaneurysms, interretinal punctuate macular edema, or of the proliferative type, characterized by neovascularization of the retina and optic disk, which may project into the vitreous, proliferation of fibrous tissue, vitreous hemorrhage, and retinal detachment. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Dialysate: A cleansing liquid used in the two major forms of dialysis--hemodialysis and peritoneal dialysis. [NIH] Dialyzer: A part of the hemodialysis machine. (See hemodialysis under dialysis.) The dialyzer has two sections separated by a membrane. One section holds dialysate. The other holds the patient's blood. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diastole: Period of relaxation of the heart, especially the ventricles. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Diastolic blood pressure: The minimum pressure that remains within the artery when the heart is at rest. [NIH] Diastolic pressure: The lowest pressure to which blood pressure falls between contractions of the ventricles. [NIH] Dichloroacetate: A derivative of acetic acid which increases the activity of pyruvate dehydrogenase and rate of lipogenesis. It is used in organic synthesis, pharmaceuticals, and medicine. [NIH] Diencephalon: The paired caudal parts of the prosencephalon from which the thalamus, hypothalamus, epithalamus, and subthalamus are derived. [NIH] Dietary Fats: Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados. [NIH]
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Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] Digitalis: A genus of toxic herbaceous Eurasian plants of the Scrophulaceae which yield cardiotonic glycosides. The most useful are Digitalis lanata and D. purpurea. [NIH] Digitalis Glycosides: Glycosides from plants of the genus Digitalis. Some of these are useful as cardiotonic and anti-arrhythmia agents. Included also are semi-synthetic derivatives of the naturally occurring glycosides. The term has sometimes been used more broadly to include all cardiac glycosides, but here is restricted to those related to Digitalis. [NIH] Dihydropyridines: Pyridine moieties which are partially saturated by the addition of two hydrogen atoms in any position. [NIH] Dihydrotestosterone: Anabolic agent. [NIH] Dilatation: The act of dilating. [NIH] Dilatation, Pathologic: The condition of an anatomical structure's being dilated beyond normal dimensions. [NIH] Dilate: Relax; expand. [NIH] Dilated cardiomyopathy: Heart muscle disease that leads to enlargement of the heart's chambers, robbing the heart of its pumping ability. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Dilator: A device used to stretch or enlarge an opening. [NIH] Diltiazem: A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of the calcium ion in membrane functions. It is also teratogenic. [NIH] Dimethyl: A volatile metabolite of the amino acid methionine. [NIH] Dipeptides: Peptides composed of two amino acid units. [NIH] Diploid: Having two sets of chromosomes. [NIH] Dipyridamole: A drug that prevents blood cell clumping and enhances the effectiveness of fluorouracil and other chemotherapeutic agents. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discrete: Made up of separate parts or characterized by lesions which do not become blended; not running together; separate. [NIH] Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Disparity: Failure of the two retinal images of an object to fall on corresponding retinal points. [NIH] Dissection: Cutting up of an organism for study. [NIH]
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Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Dissociative Disorders: Sudden temporary alterations in the normally integrative functions of consciousness. [NIH] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Diuresis: Increased excretion of urine. [EU] Diuretics, Thiazide: Diuretics characterized as analogs of 1,2,4-benzothiadiazine-1,1dioxide. All have a common mechanism of action and differ primarily in the dose required to produce a given effect. They act directly on the kidney to increase the excretion of sodium chloride and water and also increase excretion of potassium ions. [NIH] Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness. [NIH] Dobutamine: A beta-2 agonist catecholamine that has cardiac stimulant action without evoking vasoconstriction or tachycardia. It is proposed as a cardiotonic after myocardial infarction or open heart surgery. [NIH] Docosahexaenoic Acids: C22-unsaturated fatty acids found predominantly in fish oils. [NIH] Domesticated: Species in which the evolutionary process has been influenced by humans to meet their needs. [NIH] Domperidone: A specific blocker of dopamine receptors. It speeds gastrointestinal peristalsis, causes prolactin release, and is used as antiemetic and tool in the study of dopaminergic mechanisms. [NIH] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dopamine Antagonists: Drugs that bind to but do not activate dopamine receptors, thereby blocking the actions of dopamine or exogenous agonists. Many drugs used in the treatment of psychotic disorders (antipsychotic agents) are dopamine antagonists, although their therapeutic effects may be due to long-term adjustments of the brain rather than to the acute effects of blocking dopamine receptors. Dopamine antagonists have been used for several other clinical purposes including as antiemetics, in the treatment of Tourette syndrome, and for hiccup. [NIH] Dorsal: 1. Pertaining to the back or to any dorsum. 2. Denoting a position more toward the back surface than some other object of reference; same as posterior in human anatomy; superior in the anatomy of quadrupeds. [EU] Dosage schedule: A scheme set up to determine and regulate size, frequency and number of
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doses. [EU] Dose-dependent: Refers to the effects of treatment with a drug. If the effects change when the dose of the drug is changed, the effects are said to be dose dependent. [NIH] Double-blind: Pertaining to a clinical trial or other experiment in which neither the subject nor the person administering treatment knows which treatment any particular subject is receiving. [EU] Doxazosin: A selective alpha-1-adrenergic blocker that lowers serum cholesterol. It is also effective in the treatment of hypertension. [NIH] Doxycycline: A synthetic tetracycline derivative with a range of antimicrobial activity and mode of action similar to that of tetracycline, but more effective against many species. Animal studies suggest that it may cause less tooth staining than other tetracyclines. [NIH] Drip: The continuous slow introduction of a fluid containing nutrients or drugs. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Design: The molecular designing of drugs for specific purposes (such as DNAbinding, enzyme inhibition, anti-cancer efficacy, etc.) based on knowledge of molecular properties such as activity of functional groups, molecular geometry, and electronic structure, and also on information cataloged on analogous molecules. Drug design is generally computer-assisted molecular modeling and does not include pharmacokinetics, dosage analysis, or drug administration analysis. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Drug Toxicity: Manifestations of the adverse effects of drugs administered therapeutically or in the course of diagnostic techniques. It does not include accidental or intentional poisoning for which specific headings are available. [NIH] Drusen: Tiny yellow or white deposits in the retina or optic nerve head. [NIH] Dry Eye Syndrome: A common condition that occurs when the eyes do not produce enough tears to keep the eye moist and comfortable. Common symptoms of dry eye include pain, stinging, burning, scratchiness, and intermittent blurring of vision. [NIH] Duct: A tube through which body fluids pass. [NIH] Ductus Arteriosus: A fetal blood vessel connecting the pulmonary artery with the descending aorta. [NIH] Dumping Syndrome: Gastrointestinal nonfunctioning pylorus. [NIH]
symptoms
resulting
from
an
absent
or
Duodenum: The first part of the small intestine. [NIH] Dyes: Chemical substances that are used to stain and color other materials. The coloring may or may not be permanent. Dyes can also be used as therapeutic agents and test reagents in medicine and scientific research. [NIH] Dyskinesia: Impairment of the power of voluntary movement, resulting in fragmentary or incomplete movements. [EU]
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Dyslipidemia: Disorders in the lipoprotein metabolism; classified as hypercholesterolemia, hypertriglyceridemia, combined hyperlipidemia, and low levels of high-density lipoprotein (HDL) cholesterol. All of the dyslipidemias can be primary or secondary. Both elevated levels of low-density lipoprotein (LDL) cholesterol and low levels of HDL cholesterol predispose to premature atherosclerosis. [NIH] Dysmenorrhea: Painful menstruation. [NIH] Dyspareunia: Painful sexual intercourse. [NIH] Dysphoric: A feeling of unpleasantness and discomfort. [NIH] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Echocardiography: Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic. [NIH] Eclampsia: Onset of convulsions or coma in a previously diagnosed pre-eclamptic patient. [NIH]
Ectopic: Pertaining to or characterized by ectopia. [EU] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efferent: Nerve fibers which conduct impulses from the central nervous system to muscles and glands. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Effusion: The escape of fluid into a part or tissue, as an exudation or a transudation. [EU] Eicosanoids: A class of oxygenated, endogenous, unsaturated fatty acids derived from arachidonic acid. They include prostaglandins, leukotrienes, thromboxanes, and hydroxyeicosatetraenoic acid compounds (HETE). They are hormone-like substances that act near the site of synthesis without altering functions throughout the body. [NIH] Ejaculation: The release of semen through the penis during orgasm. [NIH] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Elasticity: Resistance and recovery from distortion of shape. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Electroacupuncture: A form of acupuncture using low frequency electrically stimulated needles to produce analgesia and anesthesia and to treat disease. [NIH] Electrocardiogram: Measurement of electrical activity during heartbeats. [NIH] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [NIH] Electrolysis: Destruction by passage of a galvanic electric current, as in disintegration of a chemical compound in solution. [NIH]
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Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrophoresis: An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. [NIH]
Electrophysiological: Pertaining to electrophysiology, that is a branch of physiology that is concerned with the electric phenomena associated with living bodies and involved in their functional activity. [EU] Electroplating: Coating with a metal or alloy by electrolysis. [NIH] Emboli: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embolization: The blocking of an artery by a clot or foreign material. Embolization can be done as treatment to block the flow of blood to a tumor. [NIH] Embolus: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryogenesis: The process of embryo or embryoid formation, whether by sexual (zygotic) or asexual means. In asexual embryogenesis embryoids arise directly from the explant or on intermediary callus tissue. In some cases they arise from individual cells (somatic cell embryoge). [NIH] Emergency Treatment: First aid or other immediate intervention for accidents or medical conditions requiring immediate care and treatment before definitive medical and surgical management can be procured. [NIH] Emesis: Vomiting; an act of vomiting. Also used as a word termination, as in haematemesis. [EU]
Emollient: Softening or soothing; called also malactic. [EU] Emphysema: A pathological accumulation of air in tissues or organs. [NIH] Empirical: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] Emulsion: A preparation of one liquid distributed in small globules throughout the body of a second liquid. The dispersed liquid is the discontinuous phase, and the dispersion medium is the continuous phase. When oil is the dispersed liquid and an aqueous solution is the continuous phase, it is known as an oil-in-water emulsion, whereas when water or aqueous solution is the dispersed phase and oil or oleaginous substance is the continuous phase, it is known as a water-in-oil emulsion. Pharmaceutical emulsions for which official standards have been promulgated include cod liver oil emulsion, cod liver oil emulsion with malt, liquid petrolatum emulsion, and phenolphthalein in liquid petrolatum emulsion. [EU] Enalapril: An angiotensin-converting enzyme inhibitor that is used to treat hypertension. [NIH]
Enamel: A very hard whitish substance which covers the dentine of the anatomical crown of a tooth. [NIH] Encapsulated: Confined to a specific, localized area and surrounded by a thin layer of tissue. [NIH]
Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or
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chemicals. [NIH] Endarterectomy: Surgical excision, performed under general anesthesia, of the atheromatous tunica intima of an artery. When reconstruction of an artery is performed as an endovascular procedure through a catheter, it is called atherectomy. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocardium: The innermost layer of the heart, comprised of endothelial cells. [NIH] Endocrine Glands: Ductless glands that secrete substances which are released directly into the circulation and which influence metabolism and other body functions. [NIH] Endocrine System: The system of glands that release their secretions (hormones) directly into the circulatory system. In addition to the endocrine glands, included are the chromaffin system and the neurosecretory systems. [NIH] Endocrinology: A subspecialty of internal medicine concerned with the metabolism, physiology, and disorders of the endocrine system. [NIH] Endocytosis: Cellular uptake of extracellular materials within membrane-limited vacuoles or microvesicles. Endosomes play a central role in endocytosis. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endometrial: Having to do with the endometrium (the layer of tissue that lines the uterus). [NIH]
Endometrium: The layer of tissue that lines the uterus. [NIH] Endorphin: Opioid peptides derived from beta-lipotropin. Endorphin is the most potent naturally occurring analgesic agent. It is present in pituitary, brain, and peripheral tissues. [NIH]
Endoscope: A thin, lighted tube used to look at tissues inside the body. [NIH] Endoscopic: A technique where a lateral-view endoscope is passed orally to the duodenum for visualization of the ampulla of Vater. [NIH] Endoscopy: Endoscopic examination, therapy or surgery performed on interior parts of the body. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium, Lymphatic: Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces. [NIH] Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components from interstitium to lumen; this function has been most intensively studied in the blood capillaries. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxic: Of, relating to, or acting as an endotoxin (= a heat-stable toxin, associated with the outer membranes of certain gram-negative bacteria. Endotoxins are not secreted and are released only when the cells are disrupted). [EU]
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Endotoxins: Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH] Energy balance: Energy is the capacity of a body or a physical system for doing work. Energy balance is the state in which the total energy intake equals total energy needs. [NIH] Energy Intake: Total number of calories taken in daily whether ingested or by parenteral routes. [NIH] Enhancers: Transcriptional element in the virus genome. [NIH] Enkephalins: One of the three major families of endogenous opioid peptides. The enkephalins are pentapeptides that are widespread in the central and peripheral nervous systems and in the adrenal medulla. [NIH] Enterohepatic: Of or involving the intestine and liver. [EU] Enterohepatic Circulation: Recycling through liver by excretion in bile, reabsorption from intestines into portal circulation, passage back into liver, and re-excretion in bile. [NIH] Enteropeptidase: A specialized proteolytic enzyme secreted by intestinal cells. It converts trypsinogen into its active form trypsin by removing the N-terminal peptide. EC 3.4.21.9. [NIH]
Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. [NIH] Eosinophils: Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermal Growth Factor: A 6 kD polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and
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differentiation of mesenchymal and epithelial cells. [NIH] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Epitope: A molecule or portion of a molecule capable of binding to the combining site of an antibody. For every given antigenic determinant, the body can construct a variety of antibody-combining sites, some of which fit almost perfectly, and others which barely fit. [NIH]
Epoprostenol: A prostaglandin that is biosynthesized enzymatically from prostaglandin endoperoxides in human vascular tissue. It is a potent inhibitor of platelet aggregation. The sodium salt has been also used to treat primary pulmonary hypertension. [NIH] Epoxide Hydrolases: Enzymes that catalyze reversibly the formation of an epoxide or arene oxide from a glycol or aromatic diol, respectively. EC 3.3.2.3. [NIH] Erectile: The inability to get or maintain an erection for satisfactory sexual intercourse. Also called impotence. [NIH] Erection: The condition of being made rigid and elevated; as erectile tissue when filled with blood. [EU] Ergometer: An instrument for measuring the force of muscular contraction. [NIH] Ergometry: Any method of measuring the amount of work done by an organism, usually during exertion. Ergometry also includes measures of power. Some instruments used in these determinations include the hand crank and the bicycle ergometer. [NIH] Erythrocyte Volume: Volume of circulating erythrocytes. It is usually measured by radioisotope dilution technique. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythropoietin: Glycoprotein hormone, secreted chiefly by the kidney in the adult and the liver in the fetus, that acts on erythroid stem cells of the bone marrow to stimulate proliferation and differentiation. [NIH] Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [NIH] Esophageal and Gastric Varices: Submucosal varices of the lower esophagus or gastric fundus mucosa, frequently caused by the development of portal collateral vessels consequent to portal hypertension. [NIH] Esophageal Varices: Stretched veins in the esophagus that occur when the liver is not working properly. If the veins burst, the bleeding can cause death. [NIH]
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Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Essential Tremor: A rhythmic, involuntary, purposeless, oscillating movement resulting from the alternate contraction and relaxation of opposing groups of muscles. [NIH] Estradiol: The most potent mammalian estrogenic hormone. It is produced in the ovary, placenta, testis, and possibly the adrenal cortex. [NIH] Estrogen: One of the two female sex hormones. [NIH] Estrogen receptor: ER. Protein found on some cancer cells to which estrogen will attach. [NIH]
Estrogen Replacement Therapy: The use of hormonal agents with estrogen-like activity in postmenopausal or other estrogen-deficient women to alleviate effects of hormone deficiency, such as vasomotor symptoms, dyspareunia, and progressive development of osteoporosis. This may also include the use of progestational agents in combination therapy. [NIH]
Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Ethanolamine: A viscous, hygroscopic amino alcohol with an ammoniacal odor. It is widely distributed in biological tissue and is a component of lecithin. It is used as a surfactant, fluorimetric reagent, and to remove CO2 and H2S from natural gas and other gases. [NIH] Ether: One of a class of organic compounds in which any two organic radicals are attached directly to a single oxygen atom. [NIH] Ethnic Groups: A group of people with a common cultural heritage that sets them apart from others in a variety of social relationships. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evacuation: An emptying, as of the bowels. [EU] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH] Evoked Potentials: The electric response evoked in the central nervous system by stimulation of sensory receptors or some point on the sensory pathway leading from the receptor to the cortex. The evoked stimulus can be auditory, somatosensory, or visual, although other modalities have been reported. Event-related potentials is sometimes used synonymously with evoked potentials but is often associated with the execution of a motor, cognitive, or psychophysiological task, as well as with the response to a stimulus. [NIH] Excipient: Any more or less inert substance added to a prescription in order to confer a suitable consistency or form to the drug; a vehicle. [EU] Excitability: Property of a cardiac cell whereby, when the cell is depolarized to a critical level (called threshold), the membrane becomes permeable and a regenerative inward current causes an action potential. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Excitatory: When cortical neurons are excited, their output increases and each new input they receive while they are still excited raises their output markedly. [NIH] Excitatory Amino Acids: Endogenous amino acids released by neurons as excitatory
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neurotransmitters. Glutamic acid is the most common excitatory neurotransmitter in the brain. Aspartic acid has been regarded as an excitatory transmitter for many years, but the extent of its role as a transmitter is unclear. [NIH] Excrete: To get rid of waste from the body. [NIH] Exercise Test: Controlled physical activity, more strenuous than at rest, which is performed in order to allow assessment of physiological functions, particularly cardiovascular and pulmonary, but also aerobic capacity. Maximal (most intense) exercise is usually required but submaximal exercise is also used. The intensity of exercise is often graded, using criteria such as rate of work done, oxygen consumption, and heart rate. Physiological data obtained from an exercise test may be used for diagnosis, prognosis, and evaluation of disease severity, and to evaluate therapy. Data may also be used in prescribing exercise by determining a person's exercise capacity. [NIH] Exercise Tolerance: The exercise capacity of an individual as measured by endurance (maximal exercise duration and/or maximal attained work load) during an exercise test. [NIH]
Exhaustion: The feeling of weariness of mind and body. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exocytosis: Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the cell membrane. [NIH] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exon: The part of the DNA that encodes the information for the actual amino acid sequence of the protein. In many eucaryotic genes, the coding sequences consist of a series of exons alternating with intron sequences. [NIH] Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]
Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Matrix Proteins: Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., collagen, elastin, fibronectins and laminin). [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extracorporeal: Situated or occurring outside the body. [EU] Extraction: The process or act of pulling or drawing out. [EU] Extraocular: External to or outside of the eye. [NIH] Extrapyramidal: Outside of the pyramidal tracts. [EU] Extrarenal: Outside of the kidney. [EU] Extravasation: A discharge or escape, as of blood, from a vessel into the tissues. [EU]
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Eye Infections: Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness. [NIH] Facial: Of or pertaining to the face. [EU] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Family Practice: A medical specialty concerned with the provision of continuing, comprehensive primary health care for the entire family. [NIH] Fasciculation: A small local contraction of muscles, visible through the skin, representing a spontaneous discharge of a number of fibres innervated by a single motor nerve filament. [EU]
Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Fatty Liver: The buildup of fat in liver cells. The most common cause is alcoholism. Other causes include obesity, diabetes, and pregnancy. Also called steatosis. [NIH] Fatty Liver, Alcoholic: Fatty liver in alcoholics. It is potentially reversible and may be associated with alcoholic hepatitis or cirrhosis. [NIH] Feces: The excrement discharged from the intestines, consisting of bacteria, cells exfoliated from the intestines, secretions, chiefly of the liver, and a small amount of food residue. [EU] Felodipine: A dihydropyridine calcium antagonist with positive inotropic effects. It lowers blood pressure by reducing peripheral vascular resistance through a highly selective action on smooth muscle in arteriolar resistance vessels. [NIH] Femoral: Pertaining to the femur, or to the thigh. [EU] Femoral Artery: The main artery of the thigh, a continuation of the external iliac artery. [NIH] Femur: The longest and largest bone of the skeleton, it is situated between the hip and the knee. [NIH] Fenfluramine: A centrally active drug that apparently both blocks serotonin uptake and provokes transport-mediated serotonin release. [NIH] Fertilizers: Substances or mixtures that are added to the soil to supply nutrients or to make available nutrients already present in the soil, in order to increase plant growth and productivity. [NIH] Fetal Blood: Blood of the fetus. Exchange of nutrients and waste between the fetal and maternal blood occurs via the placenta. The cord blood is blood contained in the umbilical vessels at the time of delivery. [NIH] Fetal Death: Death of the young developing in utero. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrillation: A small, local, involuntary contraction of muscle, invisible under the skin, resulting from spontaneous activation of single muscle cells or muscle fibres. [EU] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-
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identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibrinolysis: The natural enzymatic dissolution of fibrin. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibromuscular Dysplasia: An idiopathic, segmental, nonatheromatous disease of the musculature of arterial walls, leading to stenosis of small and medium-sized arteries. Most commonly affected are the renal arteries; involvement of the axillary, iliac, basilar, carotid, hepatic and intracranial arteries have been reported. [NIH] Fibronectins: Glycoproteins found on the surfaces of cells, particularly in fibrillar structures. The proteins are lost or reduced when these cells undergo viral or chemical transformation. They are highly susceptible to proteolysis and are substrates for activated blood coagulation factor VIII. The forms present in plasma are called cold-insoluble globulins. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Filtration: The passage of a liquid through a filter, accomplished by gravity, pressure, or vacuum (suction). [EU] Fish Oils: Oils high in unsaturated fats extracted from the bodies of fish or fish parts, especially the livers. Those from the liver are usually high in vitamin A. The oils are used as dietary supplements, in soaps and detergents, as protective coatings, and as a base for other food products such as vegetable shortenings. [NIH] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Flatus: Gas passed through the rectum. [NIH] Flexion: In gynaecology, a displacement of the uterus in which the organ is bent so far forward or backward that an acute angle forms between the fundus and the cervix. [EU] Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake. [NIH] Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorescent Dyes: Dyes that emit light when exposed to light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags. They are used as markers in biochemistry and immunology. [NIH] Fluorine: A nonmetallic, diatomic gas that is a trace element and member of the halogen family. It is used in dentistry as flouride to prevent dental caries. [NIH]
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Fluorouracil: A pyrimidine analog that acts as an antineoplastic antimetabolite and also has immunosuppressant. It interferes with DNA synthesis by blocking the thymidylate synthetase conversion of deoxyuridylic acid to thymidylic acid. [NIH] Flushing: A transient reddening of the face that may be due to fever, certain drugs, exertion, stress, or a disease process. [NIH] Flutter: A rapid vibration or pulsation. [EU] Folate: A B-complex vitamin that is being studied as a cancer prevention agent. Also called folic acid. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Folic Acid: N-(4-(((2-Amino-1,4-dihydro-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-Lglutamic acid. A member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. [NIH] Follicles: Shafts through which hair grows. [NIH] Folliculitis: Inflammation of follicles, primarily hair follicles. [NIH] Foramen: A natural hole of perforation, especially one in a bone. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Fosinopril: A phosphinic acid-containing angiotensin-converting enzyme inhibitor that is effective in the treatment of hypertension. It is a prodrug that is converted to its active metabolite fosinoprilat. [NIH] Fossa: A cavity, depression, or pit. [NIH] Fourth Ventricle: An irregularly shaped cavity in the rhombencephalon, between the medulla oblongata, the pons, and the isthmus in front, and the cerebellum behind. It is continuous with the central canal of the cord below and with the cerebral aqueduct above, and through its lateral and median apertures it communicates with the subarachnoid space. [NIH]
Fractionation: Dividing the total dose of radiation therapy into several smaller, equal doses delivered over a period of several days. [NIH] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH] Frontal Lobe: The anterior part of the cerebral hemisphere. [NIH] Fructose: A type of sugar found in many fruits and vegetables and in honey. Fructose is used to sweeten some diet foods. It is considered a nutritive sweetener because it has calories. [NIH] Functional Disorders: Disorders such as irritable bowel syndrome. These conditions result from poor nerve and muscle function. Symptoms such as gas, pain, constipation, and diarrhea come back again and again, but there are no signs of disease or damage. Emotional stress can trigger symptoms. Also called motility disorders. [NIH] Fundus: The larger part of a hollow organ that is farthest away from the organ's opening. The bladder, gallbladder, stomach, uterus, eye, and cavity of the middle ear all have a fundus. [NIH] Furosemide: A sulfamyl saluretic and diuretic. It has a fast onset and short duration of
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action and is used in edema and chronic renal insufficiency. [NIH] Gait: Manner or style of walking. [NIH] Gallate: Antioxidant present in tea. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gallstones: The solid masses or stones made of cholesterol or bilirubin that form in the gallbladder or bile ducts. [NIH] Gamma Rays: Very powerful and penetrating, high-energy electromagnetic radiation of shorter wavelength than that of x-rays. They are emitted by a decaying nucleus, usually between 0.01 and 10 MeV. They are also called nuclear x-rays. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] Ganglionic Blockers: Agents having as their major action the interruption of neural transmission at nicotinic receptors on postganglionic autonomic neurons. Because their actions are so broad, including blocking of sympathetic and parasympathetic systems, their therapeutic use has been largely supplanted by more specific drugs. They may still be used in the control of blood pressure in patients with acute dissecting aortic aneurysm and for the induction of hypotension in surgery. [NIH] Gap Junctions: Connections between cells which allow passage of small molecules and electric current. Gap junctions were first described anatomically as regions of close apposition between cells with a narrow (1-2 nm) gap between cell membranes. The variety in the properties of gap junctions is reflected in the number of connexins, the family of proteins which form the junctions. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gas exchange: Primary function of the lungs; transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs. [NIH] Gastrectomy: An operation to remove all or part of the stomach. [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Bypass: Surgical procedure in which the stomach is transected high on the body. The resulting proximal remnant is joined to a loop of the jejunum in an end-to-side anastomosis. This procedure is used frequently in the treatment of morbid obesity. [NIH] Gastric Fundus: The superior portion of the body of the stomach above the level of the cardiac notch. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastroenteritis: An acute inflammation of the lining of the stomach and intestines, characterized by anorexia, nausea, diarrhoea, abdominal pain, and weakness, which has various causes, including food poisoning due to infection with such organisms as Escherichia coli, Staphylococcus aureus, and Salmonella species; consumption of irritating food or drink; or psychological factors such as anger, stress, and fear. Called also
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enterogastritis. [EU] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gavage: Feeding by a tube passed into the stomach; called also tube feeding. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gels: Colloids with a solid continuous phase and liquid as the dispersed phase; gels may be unstable when, due to temperature or other cause, the solid phase liquifies; the resulting colloid is called a sol. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Deletion: A genetic rearrangement through loss of segments of DNA or RNA, bringing sequences which are normally separated into close proximity. This deletion may be detected using cytogenetic techniques and can also be inferred from the phenotype, indicating a deletion at one specific locus. [NIH] Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Expression Profiling: The determination of the pattern of genes expressed i.e., transcribed, under specific circumstances or in a specific cell. [NIH] Gene Frequency: The proportion of one particular allele in the total of all alleles for one genetic locus in a breeding population. [NIH] Gene Therapy: The introduction of new genes into cells for the purpose of treating disease by restoring or adding gene expression. Techniques include insertion of retroviral vectors, transfection, homologous recombination, and injection of new genes into the nuclei of single cell embryos. The entire gene therapy process may consist of multiple steps. The new genes may be introduced into proliferating cells in vivo (e.g., bone marrow) or in vitro (e.g., fibroblast cultures) and the modified cells transferred to the site where the gene expression is required. Gene therapy may be particularly useful for treating enzyme deficiency diseases, hemoglobinopathies, and leukemias and may also prove useful in restoring drug sensitivity, particularly for leukemia. [NIH] General practitioner: A medical practitioner who does not specialize in a particular branch of medicine or limit his practice to a specific class of diseases. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic Markers: A phenotypically recognizable genetic trait which can be used to identify a genetic locus, a linkage group, or a recombination event. [NIH] Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of
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heredity. [NIH] Genital: Pertaining to the genitalia. [EU] Genomics: The systematic study of the complete DNA sequences (genome) of organisms. [NIH]
Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Germline mutation: A gene change in the body's reproductive cells (egg or sperm) that becomes incorporated into the DNA of every cell in the body of offspring; germline mutations are passed on from parents to offspring. Also called hereditary mutation. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gestational: Psychosis attributable to or occurring during pregnancy. [NIH] Giant Cells: Multinucleated masses produced by the fusion of many cells; often associated with viral infections. In AIDS, they are induced when the envelope glycoprotein of the HIV virus binds to the CD4 antigen of uninfected neighboring T4 cells. The resulting syncytium leads to cell death and thus may account for the cytopathic effect of the virus. [NIH] Ginseng: An araliaceous genus of plants that contains a number of pharmacologically active agents used as stimulants, sedatives, and tonics, especially in traditional medicine. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glomerular Filtration Rate: The volume of water filtered out of plasma through glomerular capillary walls into Bowman's capsules per unit of time. It is considered to be equivalent to inulin clearance. [NIH] Glomeruli: Plural of glomerulus. [NIH] Glomerulonephritis: Glomerular disease characterized by an inflammatory reaction, with leukocyte infiltration and cellular proliferation of the glomeruli, or that appears to be the result of immune glomerular injury. [NIH] Glomerulosclerosis: Scarring of the glomeruli. It may result from diabetes mellitus (diabetic glomerulosclerosis) or from deposits in parts of the glomerulus (focal segmental glomerulosclerosis). The most common signs of glomerulosclerosis are proteinuria and kidney failure. [NIH] Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glottis: The vocal apparatus of the larynx, consisting of the true vocal cords (plica vocalis) and the opening between them (rima glottidis). [NIH] Glucans: Polysaccharides composed of repeating glucose units. They can consist of branched or unbranched chains in any linkages. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used
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therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] Glucose tolerance: The power of the normal liver to absorb and store large quantities of glucose and the effectiveness of intestinal absorption of glucose. The glucose tolerance test is a metabolic test of carbohydrate tolerance that measures active insulin, a hepatic function based on the ability of the liver to absorb glucose. The test consists of ingesting 100 grams of glucose into a fasting stomach; blood sugar should return to normal in 2 to 21 hours after ingestion. [NIH] Glucose Tolerance Test: Determination of whole blood or plasma sugar in a fasting state before and at prescribed intervals (usually 1/2 hr, 1 hr, 3 hr, 4 hr) after taking a specified amount (usually 100 gm orally) of glucose. [NIH] Glucuronic Acid: Derivatives of uronic acid found throughout the plant and animal kingdoms. They detoxify drugs and toxins by conjugating with them to form glucuronides in the liver which are more water-soluble metabolites that can be easily eliminated from the body. [NIH] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]
Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [NIH]
Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]
Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycolysis: The pathway by which glucose is catabolized into two molecules of pyruvic acid with the generation of ATP. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosaminoglycans: Heteropolysaccharides which contain an N-acetylated hexosamine in a characteristic repeating disaccharide unit. The repeating structure of each disaccharide involves alternate 1,4- and 1,3-linkages consisting of either N-acetylglucosamine or Nacetylgalactosamine. [NIH] Glycoside: Any compound that contains a carbohydrate molecule (sugar), particularly any such natural product in plants, convertible, by hydrolytic cleavage, into sugar and a nonsugar component (aglycone), and named specifically for the sugar contained, as glucoside (glucose), pentoside (pentose), fructoside (fructose) etc. [EU] Gonadal: Pertaining to a gonad. [EU] Gout:
Hereditary
metabolic
disorder
characterized
by
recurrent
acute
arthritis,
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hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Gp120: 120-kD HIV envelope glycoprotein which is involved in the binding of the virus to its membrane receptor, the CD4 molecule, found on the surface of certain cells in the body. [NIH]
Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Grafting: The operation of transfer of tissue from one site to another. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Grasses: A large family, Gramineae, of narrow-leaved herbaceous monocots. Many grasses produce highly allergenic pollens and are hosts to cattle parasites and toxic fungi. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Growth Plate: The area between the epiphysis and the diaphysis within which bone growth occurs. [NIH] Guanethidine: An antihypertensive agent that acts by inhibiting selectively transmission in post-ganglionic adrenergic nerves. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues. [NIH] Guanidines: A family of iminourea derivatives. The parent compound has been isolated from mushrooms, corn germ, rice hulls, mussels, earthworms, and turnip juice. Derivatives may have antiviral and antifungal properties. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Guideline Adherence: Conformity in fulfilling or following official, recognized, or institutional requirements, guidelines, recommendations, protocols, pathways, or other standards. [NIH] Guinea Pigs: A common name used for the family Caviidae. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research. [NIH]
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Habitat: An area considered in terms of its environment, particularly as this determines the type and quality of the vegetation the area can carry. [NIH] Haemodialysis: The removal of certain elements from the blood by virtue of the difference in the rates of their diffusion through a semipermeable membrane, e.g., by means of a haemodialyzer. [EU] Hair Cells: Mechanoreceptors located in the organ of Corti that are sensitive to auditory stimuli and in the vestibular apparatus that are sensitive to movement of the head. In each case the accessory sensory structures are arranged so that appropriate stimuli cause movement of the hair-like projections (stereocilia and kinocilia) which relay the information centrally in the nervous system. [NIH] Hair follicles: Shafts or openings on the surface of the skin through which hair grows. [NIH] Half-Life: The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity. [NIH] Hantavirus: A genus of the family Bunyaviridae causing Hantavirus infections, first identified during the Korean war. Infection is found primarily in rodents and humans. Transmission does not appear to involve arthropods. The genus has one recognized group (Hantaan group) consisting of several species including Dobrava-Belgrade virus, Seoul virus, Prospect Hill virus, Puumala virus, Thottapalayam virus, and Hantaan virus, the type species. [NIH] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the major histocompatibility complex. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Headache Disorders: Common conditions characterized by persistent or recurrent headaches. Headache syndrome classification systems may be based on etiology (e.g., vascular headache, post-traumatic headaches, etc.), temporal pattern (e.g., cluster headache, paroxysmal hemicrania, etc.), and precipitating factors (e.g., cough headache). [NIH] Health Behavior: Behaviors expressed by individuals to protect, maintain or promote their health status. For example, proper diet, and appropriate exercise are activities perceived to influence health status. Life style is closely associated with health behavior and factors influencing life style are socioeconomic, educational, and cultural. [NIH] Health Care Costs: The actual costs of providing services related to the delivery of health care, including the costs of procedures, therapies, and medications. It is differentiated from health expenditures, which refers to the amount of money paid for the services, and from fees, which refers to the amount charged, regardless of cost. [NIH] Health Education: Education that increases the awareness and favorably influences the attitudes and knowledge relating to the improvement of health on a personal or community basis. [NIH]
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Health Expenditures: The amounts spent by individuals, groups, nations, or private or public organizations for total health care and/or its various components. These amounts may or may not be equivalent to the actual costs (health care costs) and may or may not be shared among the patient, insurers, and/or employers. [NIH] Health Promotion: Encouraging consumer behaviors most likely to optimize health potentials (physical and psychosocial) through health information, preventive programs, and access to medical care. [NIH] Health Services: Services for the diagnosis and treatment of disease and the maintenance of health. [NIH] Health Status: The level of health of the individual, group, or population as subjectively assessed by the individual or by more objective measures. [NIH] Heart Atrium: The upper right and left chambers of the heart. [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart Catheterization: Procedure which includes placement of catheter, recording of intracardiac and intravascular pressure, obtaining blood samples for chemical analysis, and cardiac output measurement, etc. Specific angiographic injection techniques are also involved. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Heartbeat: One complete contraction of the heart. [NIH] Heart-Lung Transplantation: The simultaneous, or near simultaneous, transference of heart and lungs from one human or animal to another. [NIH] Hematology: A subspecialty of internal medicine concerned with morphology, physiology, and pathology of the blood and blood-forming tissues. [NIH] Hematoma: An extravasation of blood localized in an organ, space, or tissue. [NIH] Hematuria: Presence of blood in the urine. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemodiafiltration: The combination of hemodialysis and hemofiltration either simultaneously or sequentially. Convective transport (hemofiltration) may be better for removal of larger molecular weight substances and diffusive transport (hemodialysis) for smaller molecular weight solutes. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid. The cleaned blood then flows through another set of tubes back into the body. [NIH] Hemodilution: Reduction of blood viscosity usually by the addition of cell free solutions. Used clinically l) in states of impaired microcirculation, 2) for replacement of intraoperative blood loss without homologous blood transfusion, and 3) in cardiopulmonary bypass and hypothermia. [NIH] Hemodynamics: The movements of the blood and the forces involved in systemic or regional blood circulation. [NIH] Hemofiltration: Extracorporeal ultrafiltration technique without hemodialysis for treatment of fluid overload and electrolyte disturbances affecting renal, cardiac, or pulmonary function. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to
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hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobin E: An abnormal hemoglobin that results from the substitution of lysine for glutamic acid at position 26 of the beta chain. It is most frequently observed in southeast Asian populations. [NIH] Hemoglobin M: A group of abnormal hemoglobins in which amino acid substitutions take place in either the alpha or beta chains but near the heme iron. This results in facilitated oxidation of the hemoglobin to yield excess methemoglobin which leads to cyanosis. [NIH] Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule. [NIH] Hemoglobinuria: The presence of free hemoglobin in the urine. [NIH] Hemolytic: A disease that affects the blood and blood vessels. It destroys red blood cells, cells that cause the blood to clot, and the lining of blood vessels. HUS is often caused by the Escherichia coli bacterium in contaminated food. People with HUS may develop acute renal failure. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemorrhagic stroke: A disorder involving bleeding within ischemic brain tissue. Hemorrhagic stroke occurs when blood vessels that are damaged or dead from lack of blood supply (infarcted), located within an area of infarcted brain tissue, rupture and transform an "ischemic" stroke into a hemorrhagic stroke. Ischemia is inadequate tissue oxygenation caused by reduced blood flow; infarction is tissue death resulting from ischemia. Bleeding irritates the brain tissues, causing swelling (cerebral edema). Blood collects into a mass (hematoma). Both swelling and hematoma will compress and displace brain tissue. [NIH] Hemorrhoids: Varicosities of the hemorrhoidal venous plexuses. [NIH] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation. [NIH]
Heparin: Heparinic acid. A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts. [NIH] Hepatic: Refers to the liver. [NIH] Hepatic Artery: A branch of the celiac artery that distributes to the stomach, pancreas, duodenum, liver, gallbladder, and greater omentum. [NIH] Hepatic Veins: Veins which drain the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocytes: The main structural component of the liver. They are specialized epithelial cells that are organized into interconnected plates called lobules. [NIH] Hepatopulmonary Syndrome: A syndrome consisting of the triad of liver dysfunction,
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pulmonary vascular dilatation, and abnormal arterial oxygenation in the absence of detectable intrinsic disease of the lung and heart. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Hereditary mutation: A gene change in the body's reproductive cells (egg or sperm) that becomes incorporated into the DNA of every cell in the body of offspring; hereditary mutations are passed on from parents to offspring. Also called germline mutation. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Hernia: Protrusion of a loop or knuckle of an organ or tissue through an abnormal opening. [NIH]
Heterodimers: Zippered pair of nonidentical proteins. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Hiccup: A spasm of the diaphragm that causes a sudden inhalation followed by rapid closure of the glottis which produces a sound. [NIH] High-Frequency Jet Ventilation: Respiratory support system used primarily with rates of about 100 to 200/min with volumes of from about one to three times predicted anatomic dead space. Used to treat respiratory failure and maintain ventilation under severe circumstances. [NIH] High-Frequency Ventilation: Ventilatory support system using frequencies from 60-900 cycles/min or more. Three types of systems have been distinguished on the basis of rates, volumes, and the system used. They are high frequency positive-pressure ventilation (HFPPV), high-frequency jet ventilation (HFJV), and high-frequency oscillation (HFO). [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histamine Release: The secretion of histamine from mast cell and basophil granules by exocytosis. This can be initiated by a number of factors, all of which involve binding of IgE, cross-linked by antigen, to the mast cell or basophil's Fc receptors. Once released, histamine binds to a number of different target cell receptors and exerts a wide variety of effects. [NIH] Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [NIH] Histology: The study of tissues and cells under a microscope. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homicide: The killing of one person by another. [NIH] Homogeneous: Consisting of or composed of similar elements or ingredients; of a uniform quality throughout. [EU] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH]
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Hormone Replacement Therapy: Therapeutic use of hormones to alleviate the effects of hormone deficiency. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Humeral: 1. Of, relating to, or situated in the region of the humerus: brachial. 2. Of or belonging to the shoulder. 3. Of, relating to, or being any of several body parts that are analogous in structure, function, or location to the humerus or shoulder. [EU] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hybridomas: Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure or "monoclonal" antibodies or T-cell products, identical to those produced by the immunologically competent parent, and continually grow and divide as the neoplastic parent. [NIH] Hydralazine: A direct-acting vasodilator that is used as an antihypertensive agent. [NIH] Hydration: Combining with water. [NIH] Hydrochloric Acid: A strong corrosive acid that is commonly used as a laboratory reagent. It is formed by dissolving hydrogen chloride in water. Gastric acid is the hydrochloric acid component of gastric juice. [NIH] Hydrochlorothiazide: A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It has been used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism. [NIH] Hydrocortisone: The main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolases: Any member of the class of enzymes that catalyze the cleavage of the substrate and the addition of water to the resulting molecules, e.g., esterases, glycosidases (glycoside hydrolases), lipases, nucleotidases, peptidases (peptide hydrolases), and phosphatases (phosphoric monoester hydrolases). EC 3. [NIH]
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Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxyeicosatetraenoic Acids: Eicosatetraenoic acids substituted in any position by one or more hydroxy groups. They are important intermediates in a series of biosynthetic processes leading from arachidonic acid to a number of biologically active compounds such as prostaglandins, thromboxanes, and leukotrienes. [NIH] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hydroxyurea: An antineoplastic agent that inhibits DNA synthesis through the inhibition of ribonucleoside diphosphate reductase. [NIH] Hygienic: Pertaining to hygiene, or conducive to health. [EU] Hyperaldosteronism: Aldosteronism. [EU] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [NIH] Hypercholesterolemia: Abnormally high levels of cholesterol in the blood. [NIH] Hyperglycemia: Abnormally high blood sugar. [NIH] Hyperhomocysteinemia: An inborn error of methionone metabolism which produces an excess of homocysteine in the blood. It is often caused by a deficiency of cystathionine betasynthase and is a risk factor for coronary vascular disease. [NIH] Hyperlipidaemia: A general term for elevated concentrations of any or all of the lipids in the plasma, including hyperlipoproteinaemia, hypercholesterolaemia, etc. [EU] Hyperlipidemia: An excess of lipids in the blood. [NIH] Hyperoxaluria: Excretion of an excessive amount of oxalate in the urine. [NIH] Hyperplasia: An increase in the number of cells in a tissue or organ, not due to tumor formation. It differs from hypertrophy, which is an increase in bulk without an increase in the number of cells. [NIH] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypertension, Renal: Hypertension due to renal diseases, especially chronic parenchymal disease. Hypertension as a result of compression or obstruction of the renal artery or its branches is hypertension, renovascular. [NIH] Hypertension, Renovascular: Hypertension due to compression or obstruction of the renal artery or its branches. [NIH] Hypertensive Encephalopathy: Brain dysfunction or damage resulting from malignant hypertension, usually associated with a diastolic blood pressure in excess of 125 mmHg. Clinical manifestations include headache, nausea, emesis, seizures, altered mental status (in some cases progressing to coma), papilledema, and retinal hemorrhage. Focal neurologic signs may develop. Pathologically, this condition may be associated with the formation of ischemic lesions in the brain (brain ischemia). [NIH]
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Hyperthyroidism: Excessive functional activity of the thyroid gland. [NIH] Hypertriglyceridemia: Condition of elevated triglyceride concentration in the blood; an inherited form occurs in familial hyperlipoproteinemia IIb and hyperlipoproteinemia type IV. It has been linked to higher risk of heart disease and arteriosclerosis. [NIH] Hypertrophic cardiomyopathy: Heart muscle disease that leads to thickening of the heart walls, interfering with the heart's ability to fill with and pump blood. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hyperuricemia: A buildup of uric acid (a byproduct of metabolism) in the blood; a side effect of some anticancer drugs. [NIH] Hypnotic: A drug that acts to induce sleep. [EU] Hypoglycaemia: An abnormally diminished concentration of glucose in the blood, which may lead to tremulousness, cold sweat, piloerection, hypothermia, and headache, accompanied by irritability, confusion, hallucinations, bizarre behaviour, and ultimately, convulsions and coma. [EU] Hypoglycemia: Abnormally low blood sugar [NIH] Hypoplasia: Incomplete development or underdevelopment of an organ or tissue. [EU] Hypotension: Abnormally low blood pressure. [NIH] Hypotensive: Characterized by or causing diminished tension or pressure, as abnormally low blood pressure. [EU] Hypothalamic: Of or involving the hypothalamus. [EU] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hypothermia: Lower than normal body temperature, especially in warm-blooded animals; in man usually accidental or unintentional. [NIH] Hypoventilation: A reduction in the amount of air entering the pulmonary alveoli. [NIH] Hypoxanthine: A purine and a reaction intermediate in the metabolism of adenosine and in the formation of nucleic acids by the salvage pathway. [NIH] Hypoxemia: Deficient oxygenation of the blood; hypoxia. [EU] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Hypoxic: Having too little oxygen. [NIH] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Ileum: The lower end of the small intestine. [NIH] Iloprost: An eicosanoid, derived from the cyclooxygenase pathway of arachidonic acid metabolism. It is a stable and synthetic analog of epoprostenol, but with a longer half-life than the parent compound. Its actions are similar to prostacyclin. Iloprost produces vasodilation and inhibits platelet aggregation. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Immersion: The placing of a body or a part thereof into a liquid. [NIH] Immune response: The activity of the immune system against foreign substances (antigens).
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[NIH]
Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]
effects
of
foreign
Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunoassay: Immunochemical assay or detection of a substance by serologic or immunologic methods. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunodeficiency syndrome: The inability of the body to produce an immune response. [NIH]
Immunogenic: Producing immunity; evoking an immune response. [EU] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunophilin: A drug for the treatment of Parkinson's disease. [NIH] Immunosuppressant: An agent capable of suppressing immune responses. [EU] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] Impotence: The inability to perform sexual intercourse. [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes. [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence)
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or the escape of stool from the rectum (fecal incontinence). [NIH] Incubation: The development of an infectious disease from the entrance of the pathogen to the appearance of clinical symptoms. [EU] Incubation period: The period of time likely to elapse between exposure to the agent of the disease and the onset of clinical symptoms. [NIH] Indapamide: A sulfamyl diuretic with about 16x the effect of furosemide. It has also been shown to be an effective antihypertensive agent in the clinic. [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes. [NIH] Indoramin: A hypotensive agent with some anti-arrhythmic effects. [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infant Mortality: Perinatal, neonatal, and infant deaths in a given population. [NIH] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Inferior vena cava: A large vein that empties into the heart. It carries blood from the legs and feet, and from organs in the abdomen and pelvis. [NIH] Infertility: The diminished or absent ability to conceive or produce an offspring while sterility is the complete inability to conceive or produce an offspring. [NIH] Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH]
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Innervation: 1. The distribution or supply of nerves to a part. 2. The supply of nervous energy or of nerve stimulus sent to a part. [EU] Inorganic: Pertaining to substances not of organic origin. [EU] Inotropic: Affecting the force or energy of muscular contractions. [EU] Inpatients: Persons admitted to health facilities which provide board and room, for the purpose of observation, care, diagnosis or treatment. [NIH] Insecticides: Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insomnia: Difficulty in going to sleep or getting enough sleep. [NIH] Instillation: . [EU] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Integrins: A family of transmembrane glycoproteins consisting of noncovalent heterodimers. They interact with a wide variety of ligands including extracellular matrix glycoproteins, complement, and other cells, while their intracellular domains interact with the cytoskeleton. The integrins consist of at least three identified families: the cytoadhesin receptors, the leukocyte adhesion receptors, and the very-late-antigen receptors. Each family contains a common beta-subunit combined with one or more distinct alpha-subunits. These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development, hemostasis, thrombosis, wound healing, immune and nonimmune defense mechanisms, and oncogenic transformation. [NIH] Intensive Care: Advanced and highly specialized care provided to medical or surgical patients whose conditions are life-threatening and require comprehensive care and constant monitoring. It is usually administered in specially equipped units of a health care facility. [NIH]
Intensive Care Units: Hospital units providing continuous surveillance and care to acutely ill patients. [NIH] Interindividual: Occurring between two or more individuals. [EU] Interleukin-6: Factor that stimulates the growth and differentiation of human B-cells and is also a growth factor for hybridomas and plasmacytomas. It is produced by many different cells including T-cells, monocytes, and fibroblasts. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults. [NIH] Interneurons: Most generally any neurons which are not motor or sensory. Interneurons
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may also refer to neurons whose axons remain within a particular brain region as contrasted with projection neurons which have axons projecting to other brain regions. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intestinal: Having to do with the intestines. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intracellular Membranes: Membranes of subcellular structures. [NIH] Intracranial Aneurysm: A saclike dilatation of the walls of a blood vessel, usually an artery. [NIH]
Intracranial Hypertension: Increased pressure within the cranial vault. This may result from several conditions, including hydrocephalus; brain edema; intracranial masses; severe systemic hypertension; pseudotumor cerebri; and other disorders. [NIH] Intracranial Pressure: Pressure within the cranial cavity. It is influenced by brain mass, the circulatory system, CSF dynamics, and skull rigidity. [NIH] Intrahepatic: Within the liver. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intramuscular injection: IM. Injection into a muscle. [NIH] Intraocular: Within the eye. [EU] Intraocular pressure: Pressure of the fluid inside the eye; normal IOP varies among individuals. [NIH] Intravascular: Within a vessel or vessels. [EU] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Intubation: Introduction of a tube into a hollow organ to restore or maintain patency if obstructed. It is differentiated from catheterization in that the insertion of a catheter is usually performed for the introducing or withdrawing of fluids from the body. [NIH] Inulin: A starch found in the tubers and roots of many plants. Since it is hydrolyzable to fructose, it is classified as a fructosan. It has been used in physiologic investigation for determination of the rate of glomerular function. [NIH] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Involuntary: Reaction occurring without intention or volition. [NIH] Involution: 1. A rolling or turning inward. 2. One of the movements involved in the gastrulation of many animals. 3. A retrograde change of the entire body or in a particular organ, as the retrograde changes in the female genital organs that result in normal size after delivery. 4. The progressive degeneration occurring naturally with advancing age, resulting in shrivelling of organs or tissues. [EU] Iodine: A nonmetallic element of the halogen group that is represented by the atomic symbol I, atomic number 53, and atomic weight of 126.90. It is a nutritionally essential element, especially important in thyroid hormone synthesis. In solution, it has anti-infective properties and is used topically. [NIH]
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Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for channel gating can be a membrane potential, drug, transmitter, cytoplasmic messenger, or a mechanical deformation. Ion channels which are integral parts of ionotropic neurotransmitter receptors are not included. [NIH] Ion Pumps: Integral membrane proteins that transport ions across a membrane against an electrochemical gradient. [NIH] Ion Transport: The movement of ions across energy-transducing cell membranes. Transport can be active or passive. Passive ion transport (facilitated diffusion) derives its energy from the concentration gradient of the ion itself and allows the transport of a single solute in one direction (uniport). Active ion transport is usually coupled to an energy-yielding chemical or photochemical reaction such as ATP hydrolysis. This form of primary active transport is called an ion pump. Secondary active transport utilizes the voltage and ion gradients produced by the primary transport to drive the cotransport of other ions or molecules. These may be transported in the same (symport) or opposite (antiport) direction. [NIH] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Iris: The most anterior portion of the uveal layer, separating the anterior chamber from the posterior. It consists of two layers - the stroma and the pigmented epithelium. Color of the iris depends on the amount of melanin in the stroma on reflection from the pigmented epithelium. [NIH] Irritants: Drugs that act locally on cutaneous or mucosal surfaces to produce inflammation; those that cause redness due to hyperemia are rubefacients; those that raise blisters are vesicants and those that penetrate sebaceous glands and cause abscesses are pustulants; tear gases and mustard gases are also irritants. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Ischemic stroke: A condition in which the blood supply to part of the brain is cut off. Also called "plug-type" strokes. Blocked arteries starve areas of the brain controlling sight, speech, sensation, and movement so that these functions are partially or completely lost. Ischemic stroke is the most common type of stroke, accounting for 80 percent of all strokes. Most ischemic strokes are caused by a blood clot called a thrombus, which blocks blood flow in the arteries feeding the brain, usually the carotid artery in the neck, the major vessel bringing blood to the brain. When it becomes blocked, the risk of stroke is very high. [NIH] Islet: Cell producing insulin in pancreas. [NIH] Isometric Contraction: Muscular contractions characterized by increase in tension without change in length. [NIH] Isopropyl: A gene mutation inducer. [NIH] Isoproterenol: Isopropyl analog of epinephrine; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant. [NIH] Isosorbide: 1,4:3,6-Dianhydro D-glucitol. Chemically inert osmotic diuretic used mainly to treat hydrocephalus; also used in glaucoma. [NIH] Isosorbide Dinitrate: A vasodilator used in the treatment of angina. Its actions are similar to nitroglycerin but with a slower onset of action. [NIH]
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Isotonic: A biological term denoting a solution in which body cells can be bathed without a net flow of water across the semipermeable cell membrane. Also, denoting a solution having the same tonicity as some other solution with which it is compared, such as physiologic salt solution and the blood serum. [EU] Jaundice: A clinical manifestation of hyperbilirubinemia, consisting of deposition of bile pigments in the skin, resulting in a yellowish staining of the skin and mucous membranes. [NIH]
Jejunum: That portion of the small intestine which extends from the duodenum to the ileum; called also intestinum jejunum. [EU] Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Kallidin: A decapeptide bradykinin homolog produced by the action of tissue and glandular kallikreins on low-molecular-weight kininogen. It is a smooth-muscle stimulant and hypotensive agent that functions through vasodilatation. [NIH] Kallikrein-Kinin System: A system produced in the distal nephron of the kidney. Its components are kallikrein, kinins, kininase I and II, and enkephalinase. It is involved in mediation and modulation of the renin-angiotensin-aldosterone system, prostaglandins, vasopressins, and in the regulation of sodium-water balance, renal hemodynamics, and particularly blood pressure. The system participates in the control of renal functions and the physiopathology of renal diseases. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keratolytic: An agent that promotes keratolysis. [EU] Keto: It consists of 8 carbon atoms and within the endotoxins, it connects poysaccharide and lipid A. [NIH] Kidney Cortex: The outer zone of the kidney, beneath the capsule, consisting of kidney glomerulus; kidney tubules, distal; and kidney tubules, proximal. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kidney Failure: The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH] Kidney Failure, Acute: A clinical syndrome characterized by a sudden decrease in glomerular filtration rate, often to values of less than 1 to 2 ml per minute. It is usually associated with oliguria (urine volumes of less than 400 ml per day) and is always associated with biochemical consequences of the reduction in glomerular filtration rate such as a rise in blood urea nitrogen (BUN) and serum creatinine concentrations. [NIH] Kidney Failure, Chronic: An irreversible and usually progressive reduction in renal function in which both kidneys have been damaged by a variety of diseases to the extent that they are unable to adequately remove the metabolic products from the blood and regulate the body's electrolyte composition and acid-base balance. Chronic kidney failure requires hemodialysis or surgery, usually kidney transplantation. [NIH] Kidney Glomerulus: A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue. [NIH]
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Kidney stone: A stone that develops from crystals that form in urine and build up on the inner surfaces of the kidney, in the renal pelvis, or in the ureters. [NIH] Kidney Transplantation: The transference of a kidney from one human or animal to another. [NIH] Kinetics: The study of rate dynamics in chemical or physical systems. [NIH] Labetalol: Blocker of both alpha- and beta-adrenergic receptors that is used as an antihypertensive. [NIH] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lactation: The period of the secretion of milk. [EU] Lactococcus: A genus of gram-positive, coccoid bacteria mainly isolated from milk and milk products. These bacteria are also found in plants and nonsterile frozen and dry foods. Previously thought to be a member of the genus Streptococcus (group N), it is now recognized as a separate genus. [NIH] Lactococcus lactis: A non-pathogenic lactococcus found in dairy products and responsible for the souring of milk. [NIH] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Larynx: An irregularly shaped, musculocartilaginous tubular structure, lined with mucous membrane, located at the top of the trachea and below the root of the tongue and the hyoid bone. It is the essential sphincter guarding the entrance into the trachea and functioning secondarily as the organ of voice. [NIH] Latency: The period of apparent inactivity between the time when a stimulus is presented and the moment a response occurs. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Least-Squares Analysis: A principle of estimation in which the estimates of a set of parameters in a statistical model are those quantities minimizing the sum of squared differences between the observed values of a dependent variable and the values predicted by the model. [NIH] Lectin: A complex molecule that has both protein and sugars. Lectins are able to bind to the outside of a cell and cause biochemical changes in it. Lectins are made by both animals and plants. [NIH] Leisure Activities: Voluntary use of free time for activities outside the daily routine. [NIH] Lens: The transparent, double convex (outward curve on both sides) structure suspended between the aqueous and vitreous; helps to focus light on the retina. [NIH] Lentivirus: A genus of the family Retroviridae consisting of non-oncogenic retroviruses that produce multi-organ diseases characterized by long incubation periods and persistent infection. Lentiviruses are unique in that they contain open reading frames (ORFs) between the pol and env genes and in the 3' env region. Five serogroups are recognized, reflecting the mammalian hosts with which they are associated. HIV-1 is the type species. [NIH]
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Leptin: A 16-kD peptide hormone secreted from white adipocytes and implicated in the regulation of food intake and energy balance. Leptin provides the key afferent signal from fat cells in the feedback system that controls body fat stores. [NIH] Lethal: Deadly, fatal. [EU] Lethargy: Abnormal drowsiness or stupor; a condition of indifference. [EU] Leucine: An essential branched-chain amino acid important for hemoglobin formation. [NIH] Leucocyte: All the white cells of the blood and their precursors (myeloid cell series, lymphoid cell series) but commonly used to indicate granulocytes exclusive of lymphocytes. [NIH]
Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Libido: The psychic drive or energy associated with sexual instinct in the broad sense (pleasure and love-object seeking). It may also connote the psychic energy associated with instincts in general that motivate behavior. [NIH] Library Services: Services offered to the library user. They include reference and circulation. [NIH]
Life Expectancy: A figure representing the number of years, based on known statistics, to which any person of a given age may reasonably expect to live. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] Ligase: An enzyme that repairs single stranded discontinuities in double-stranded DNA molecules in the cell. Purified DNA ligase is used in gene cloning to join DNA molecules together. [NIH] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Likelihood Functions: Functions constructed from a statistical model and a set of observed data which give the probability of that data for various values of the unknown model parameters. Those parameter values that maximize the probability are the maximum likelihood estimates of the parameters. [NIH] Lincomycin: (2S-trans)-Methyl 6,8-dideoxy-6-(((1-methyl-4-propyl-2pyrrolidinyl)carbonyl)amino)-1-thio-D-erythro-alpha-D-galacto-octopyranoside. An antibiotic produced by Streptomyces lincolnensis var. lincolnensis. It has been used in the treatment of staphylococcal, streptococcal, and Bacteroides fragilis infections. [NIH] Linear Models: Statistical models in which the value of a parameter for a given value of a factor is assumed to be equal to a + bx, where a and b are constants. The models predict a linear regression. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH]
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Linkage Disequilibrium: Nonrandom association of linked genes. This is the tendency of the alleles of two separate but already linked loci to be found together more frequently than would be expected by chance alone. [NIH] Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3. [NIH] Lipid: Fat. [NIH] Lipid A: Lipid A is the biologically active component of lipopolysaccharides. It shows strong endotoxic activity and exhibits immunogenic properties. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipophilic: Having an affinity for fat; pertaining to or characterized by lipophilia. [EU] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Lipoprotein Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34. [NIH] Lipoprotein(a): A family of lipoprotein particles varying in density and size depending on the protein-lipid ratio and the protein composition. These particles consist of apolipoprotein B-100 covalently linked to apolipoprotein-a by one or two disulfide bonds. There is a correlation between high plasma levels of this lipoprotein and increased risk for atherosclerotic cardiovascular disease. [NIH] Liposome: A spherical particle in an aqueous medium, formed by a lipid bilayer enclosing an aqueous compartment. [EU] Lipoxygenase: An enzyme of the oxidoreductase class that catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives. Related enzymes in this class include the arachidonate lipoxygenases, arachidonate 5lipoxygenase, arachidonate 12-lipoxygenase, and arachidonate 15-lipoxygenase. EC 1.13.11.12. [NIH] Lisinopril: An orally active angiotensin-converting enzyme inhibitor that has been used in the treatment of hypertension and congestive heart failure. [NIH] Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight 6.94. Salts of lithium are used in treating manic-depressive disorders. [NIH]
Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver Cirrhosis: Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules. [NIH]
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Liver scan: An image of the liver created on a computer screen or on film. A radioactive substance is injected into a blood vessel and travels through the bloodstream. It collects in the liver, especially in abnormal areas, and can be detected by the scanner. [NIH] Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH] Lobe: A portion of an organ such as the liver, lung, breast, or brain. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Logistic Models: Statistical models which describe the relationship between a qualitative dependent variable (that is, one which can take only certain discrete values, such as the presence or absence of a disease) and an independent variable. A common application is in epidemiology for estimating an individual's risk (probability of a disease) as a function of a given risk factor. [NIH] Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [NIH] Long-Term Care: Care over an extended period, usually for a chronic condition or disability, requiring periodic, intermittent, or continuous care. [NIH] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside diameter) and used in transferring microorganisms. [NIH] Low vision: Visual loss that cannot be corrected with eyeglasses or contact lenses and interferes with daily living activities. [NIH] Low-density lipoprotein: Lipoprotein that contains most of the cholesterol in the blood. LDL carries cholesterol to the tissues of the body, including the arteries. A high level of LDL increases the risk of heart disease. LDL typically contains 60 to 70 percent of the total serum cholesterol and both are directly correlated with CHD risk. [NIH] Lower Body Negative Pressure: External decompression applied to the lower body. It is used to study orthostatic intolerance and the effects of gravitation and acceleration, to produce simulated hemorrhage in physiologic research, to assess cardiovascular function, and to reduce abdominal stress during childbirth. [NIH] Lubricants: Oily or slippery substances. [NIH] Luciferase: Any one of several enzymes that catalyze the bioluminescent reaction in certain marine crustaceans, fish, bacteria, and insects. The enzyme is a flavoprotein; it oxidizes luciferins to an electronically excited compound that emits energy in the form of light. The color of light emitted varies with the organism. The firefly enzyme is a valuable reagent for measurement of ATP concentration. (Dorland, 27th ed) EC 1.13.12.-. [NIH] Lumbar: Pertaining to the loins, the part of the back between the thorax and the pelvis. [EU] Lumen: The cavity or channel within a tube or tubular organ. [EU]
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Lung Transplantation: The transference of either one or both of the lungs from one human or animal to another. [NIH] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphoblastic: One of the most aggressive types of non-Hodgkin lymphoma. [NIH] Lymphoblasts: Interferon produced predominantly by leucocyte cells. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphokines: Soluble protein factors generated by activated lymphocytes that affect other cells, primarily those involved in cellular immunity. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Macrophage Activation: The process of altering the morphology and functional activity of macrophages so that they become avidly phagocytic. It is initiated by lymphokines, such as the macrophage activation factor (MAF) and the macrophage migration-inhibitory factor (MMIF), immune complexes, C3b, and various peptides, polysaccharides, and immunologic adjuvants. [NIH] Macula: A stain, spot, or thickening. Often used alone to refer to the macula retinae. [EU] Macula Lutea: An oval area in the retina, 3 to 5 mm in diameter, usually located temporal to the superior pole of the eye and slightly below the level of the optic disk. [NIH] Macular Degeneration: Degenerative changes in the macula lutea of the retina. [NIH] Magnetic Resonance Angiography: Non-invasive method of vascular imaging and determination of internal anatomy without injection of contrast media or radiation exposure. The technique is used especially in cerebral angiography as well as for studies of other vascular structures. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH]
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Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) transplantation antigens, genes which control the structure of the immune responseassociated (Ia) antigens, the immune response (Ir) genes which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement. [NIH] Malabsorption: Impaired intestinal absorption of nutrients. [EU] Malformation: A morphologic developmental process. [EU]
defect
resulting
from
an
intrinsically
abnormal
Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant tumor: A tumor capable of metastasizing. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Mammary: Pertaining to the mamma, or breast. [EU] Mandible: The largest and strongest bone of the face constituting the lower jaw. It supports the lower teeth. [NIH] Manic: Affected with mania. [EU] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Marital Status: A demographic parameter indicating a person's status with respect to marriage, divorce, widowhood, singleness, etc. [NIH] Mastication: The act and process of chewing and grinding food in the mouth. [NIH] Matrix metalloproteinase: A member of a group of enzymes that can break down proteins, such as collagen, that are normally found in the spaces between cells in tissues (i.e., extracellular matrix proteins). Because these enzymes need zinc or calcium atoms to work properly, they are called metalloproteinases. Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis. [NIH] Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]
Meat Products: Articles of food which are derived by a process of manufacture from any portion of carcasses of any animal used for food (e.g., head cheese, sausage, scrapple). [NIH] Meatus: A canal running from the internal auditory foramen through the petrous portion of the temporal bone. It gives passage to the facial and auditory nerves together with the auditory branch of the basilar artery and the internal auditory veins. [NIH] Mechanoreceptors: Cells specialized to transduce mechanical stimuli and relay that information centrally in the nervous system. Mechanoreceptors include hair cells, which mediate hearing and balance, and the various somatosensory receptors, often with nonneural accessory structures. [NIH] Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen
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with antibody or by the action of antigen with a sensitized lymphocyte. [EU] Medical Records: Recording of pertinent information concerning patient's illness or illnesses. [NIH] Medicament: A medicinal substance or agent. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Medullary: Pertaining to the marrow or to any medulla; resembling marrow. [EU] Megaloblastic: A large abnormal red blood cell appearing in the blood in pernicious anaemia. [EU] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Melanin: The substance that gives the skin its color. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Glycoproteins: Glycoproteins found on the membrane or surface of cells. [NIH] Membrane Lipids: Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation. [NIH] Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningioma: A type of tumor that occurs in the meninges, the membranes that cover and protect the brain and spinal cord. Meningiomas usually grow slowly. [NIH] Menopause: Permanent cessation of menstruation. [NIH] Menstrual Cycle: The period of the regularly recurring physiologic changes in the endometrium occurring during the reproductive period in human females and some primates and culminating in partial sloughing of the endometrium (menstruation). [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal tissues from the nonpregnant uterus. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior
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producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Mesenchymal: Refers to cells that develop into connective tissue, blood vessels, and lymphatic tissue. [NIH] Mesenteric: Pertaining to the mesentery : a membranous fold attaching various organs to the body wall. [EU] Mesenteric Arteries: Arteries which arise from the abdominal aorta and distribute to most of the intestines. [NIH] Mesenteric Veins: Veins which return blood from the intestines; the inferior mesenteric vein empties into the splenic vein, the superior mesenteric vein joins the splenic vein to form the portal vein. [NIH] Mesentery: A layer of the peritoneum which attaches the abdominal viscera to the abdominal wall and conveys their blood vessels and nerves. [NIH] Meta-Analysis: A quantitative method of combining the results of independent studies (usually drawn from the published literature) and synthesizing summaries and conclusions which may be used to evaluate therapeutic effectiveness, plan new studies, etc., with application chiefly in the areas of research and medicine. [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metaplasia: A condition in which there is a change of one adult cell type to another similar adult cell type. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Methanol: A colorless, flammable liquid used in the manufacture of formaldehyde and acetic acid, in chemical synthesis, antifreeze, and as a solvent. Ingestion of methanol is toxic and may cause blindness. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] Methyldopa: An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent. Before its alphaadrenergic actions became clear, methyldopa was thought to act by inhibiting decarboxylation of DOPA leading to depletion of norepinephrine or by conversion to and release as the false transmitter alpha-methylnorepinephrine. [NIH] Metoclopramide: A dopamine D2 antagonist that is used as an antiemetic. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH]
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Mibefradil: A benzimidazoyl-substituted tetraline that binds selectively to and inhibits calcium channels, T-type. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microcirculation: The vascular network lying between the arterioles and venules; includes capillaries, metarterioles and arteriovenous anastomoses. Also, the flow of blood through this network. [NIH] Microdialysis: A technique for measuring extracellular concentrations of substances in tissues, usually in vivo, by means of a small probe equipped with a semipermeable membrane. Substances may also be introduced into the extracellular space through the membrane. [NIH] Microglia: The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Micro-organism: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Microsomal: Of or pertaining to microsomes : vesicular fragments of endoplasmic reticulum formed after disruption and centrifugation of cells. [EU] Microspheres: Small uniformly-sized spherical particles frequently radioisotopes or various reagents acting as tags or markers. [NIH]
labeled
with
Midodrine: An ethanolamine derivative that is an adrenergic alpha agonist. It is used as a vasoconstrictor agent in the treatment of hypotension. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Milliliter: A measure of volume for a liquid. A milliliter is approximately 950-times smaller than a quart and 30-times smaller than a fluid ounce. A milliliter of liquid and a cubic centimeter (cc) of liquid are the same. [NIH] Millimeter: A measure of length. A millimeter is approximately 26-times smaller than an inch. [NIH] Mineralocorticoid: 1. Any of the group of C21 corticosteroids, principally aldosterone, predominantly involved in the regulation of electrolyte and water balance through their effect on ion transport in epithelial cells of the renal tubules, resulting in retention of sodium and loss of potassium; some also possess varying degrees of glucocorticoid activity. Their secretion is regulated principally by plasma volume, serum potassium concentration and angiotensin II, and to a lesser extent by anterior pituitary ACTH. 2. Of, pertaining to, having
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the properties of, or resembling a mineralocorticoid. [EU] Miosis: Pupillary constriction. This may result from congenital absence of the dilatator pupillary muscle, defective sympathetic innervation, or irritation of the conjunctiva or cornea. [NIH] Miotic: 1. Pertaining to, characterized by, or producing miosis : contraction of the pupil. 2. An agent that causes the pupil to contract. 3. Meiotic: characterized by cell division. [EU] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mobilization: The process of making a fixed part or stored substance mobile, as by separating a part from surrounding structures to make it accessible for an operative procedure or by causing release into the circulation for body use of a substance stored in the body. [EU] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Modulator: A specific inductor that brings out characteristics peculiar to a definite region. [EU]
Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecular Probes: A group of atoms or molecules attached to other molecules or cellular structures and used in studying the properties of these molecules and structures. Radioactive DNA or RNA sequences are used in molecular genetics to detect the presence of a complementary sequence by molecular hybridization. [NIH] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoamine: Enzyme that breaks down dopamine in the astrocytes and microglia. [NIH] Monoamine Oxidase: An enzyme that catalyzes the oxidative deamination of naturally occurring monoamines. It is a flavin-containing enzyme that is localized in mitochondrial membranes, whether in nerve terminals, the liver, or other organs. Monoamine oxidase is important in regulating the metabolic degradation of catecholamines and serotonin in neural or target tissues. Hepatic monoamine oxidase has a crucial defensive role in inactivating circulating monoamines or those, such as tyramine, that originate in the gut and are absorbed into the portal circulation. (From Goodman and Gilman's, The Pharmacological Basis of Therapeutics, 8th ed, p415) EC 1.4.3.4. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH]
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Monocrotaline: A pyrrolizidine alkaloid and a toxic plant constituent that poisons livestock and humans through the ingestion of contaminated grains and other foods. The alkaloid causes pulmonary artery hypertension, right ventricular hypertrophy, and pathological changes in the pulmonary vasculature. Significant attenuation of the cardiopulmonary changes are noted after oral magnesium treatment. [NIH] Monocyte: A type of white blood cell. [NIH] Monogenic: A human disease caused by a mutation in a single gene. [NIH] Monotherapy: A therapy which uses only one drug. [EU] Morphine: The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motility: The ability to move spontaneously. [EU] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [NIH] Motor Activity: The physical activity of an organism as a behavioral phenomenon. [NIH] Mucinous: Containing or resembling mucin, the main compound in mucus. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [NIH] Multicenter study: A clinical trial that is carried out at more than one medical institution. [NIH]
Multicystic Dysplastic Kidney: A severe form of dysplasia where the kidney typically appears as a bunch of grapes without a reniform configuration or calyceal drainage system. It occurs in-utero and is the most common form of nongenetic renal cystic disease. [NIH] Multiple Myeloma: A malignant tumor of plasma cells usually arising in the bone marrow; characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria, and anemia. [NIH] Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Muscle Fibers: Large single cells, either cylindrical or prismatic in shape, that form the basic unit of muscle tissue. They consist of a soft contractile substance enclosed in a tubular sheath. [NIH] Muscle Hypertonia: Abnormal increase in skeletal or smooth muscle tone. Skeletal muscle hypertonicity may be associated with pyramidal tract lesions or basal ganglia diseases. [NIH] Muscle Relaxation: That phase of a muscle twitch during which a muscle returns to a resting position. [NIH] Muscular Atrophy: Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are
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characterized by progressive degeneration of skeletal muscles. [NIH] Musculature: The muscular apparatus of the body, or of any part of it. [EU] Mustard Gas: Severe irritant and vesicant of skin, eyes, and lungs. It may cause blindness and lethal lung edema and was formerly used as a war gas. The substance has been proposed as a cytostatic and for treatment of psoriasis. It has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP-85-002, 1985) (Merck, 11th ed). [NIH] Mydriasis: Dilation of pupils to greater than 6 mm combined with failure of the pupils to constrict when stimulated with light. This condition may occur due to injury of the pupillary fibers in the oculomotor nerve, in acute angle-closure glaucoma, and in Adie syndrome. [NIH]
Mydriatic: 1. Dilating the pupil. 2. Any drug that dilates the pupil. [EU] Myelin: The fatty substance that covers and protects nerves. [NIH] Myelofibrosis: A disorder in which the bone marrow is replaced by fibrous tissue. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardial Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary arteriosclerosis), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (myocardial infarction). [NIH] Myocardial Reperfusion: Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing myocardial reperfusion injury. [NIH] Myocardial Reperfusion Injury: Functional, metabolic, or structural changes in ischemic heart muscle thought to result from reperfusion to the ischemic areas. Changes can be fatal to muscle cells and may include edema with explosive cell swelling and disintegration, sarcolemma disruption, fragmentation of mitochondria, contraction band necrosis, enzyme washout, and calcium overload. Other damage may include hemorrhage and ventricular arrhythmias. One possible mechanism of damage is thought to be oxygen free radicals. Treatment currently includes the introduction of scavengers of oxygen free radicals, and injury is thought to be prevented by warm blood cardioplegic infusion prior to reperfusion. [NIH]
Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myosin: Chief protein in muscle and the main constituent of the thick filaments of muscle fibers. In conjunction with actin, it is responsible for the contraction and relaxation of muscles. [NIH] Myotonic Dystrophy: A condition presenting muscle weakness and wasting which may be progressive. [NIH] Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors. [NIH]
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Naltrexone: Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of naloxone. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence. [NIH] Naphthalenes: Two-ring crystalline hydrocarbons isolated from coal tar. They are used as intermediates in chemical synthesis, as insect repellents, fungicides, lubricants, preservatives, and, formerly, as topical antiseptics. [NIH] Narcosis: A general and nonspecific reversible depression of neuronal excitability, produced by a number of physical and chemical aspects, usually resulting in stupor. [NIH] Narcotic: 1. Pertaining to or producing narcosis. 2. An agent that produces insensibility or stupor, applied especially to the opioids, i.e. to any natural or synthetic drug that has morphine-like actions. [EU] Natriuresis: The excretion of abnormal amounts of sodium in the urine. [EU] Natriuretic Hormone: A low-molecular weight substance, possibly from the hypothalamus, which is released due to plasma volume expansion. It causes natriuresis in part by inhibiting sodium potassium ATPase. The development of hypertension may be the consequence of an abnormality in volume regulation induced by a defect in the renal response to the natriuretic effect of the natriuretic hormone. Do not confuse with atrial natriuretic factor or cardionatrin which is a different, well characterized hormone. [NIH] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Near Drowning: Non-fatal immersion or submersion in water. The subject is resuscitable. [NIH]
Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Needs Assessment: Systematic identification of a population's needs or the assessment of individuals to determine the proper level of services needed. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neonatal period: The first 4 weeks after birth. [NIH] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasms: New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephrectomy: Surgery to remove a kidney. Radical nephrectomy removes the kidney, the adrenal gland, nearby lymph nodes, and other surrounding tissue. Simple nephrectomy removes only the kidney. Partial nephrectomy removes the tumor but not the entire kidney. [NIH]
Nephritis: Inflammation of the kidney; a focal or diffuse proliferative or destructive process which may involve the glomerulus, tubule, or interstitial renal tissue. [EU]
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Nephrogenic: Constant thirst and frequent urination because the kidney tubules cannot respond to antidiuretic hormone. The result is an increase in urine formation and excessive urine flow. [NIH] Nephrologist: A doctor who treats patients with kidney problems or hypertension. [NIH] Nephrology: A subspecialty of internal medicine concerned with the anatomy, physiology, and pathology of the kidney. [NIH] Nephron: A tiny part of the kidneys. Each kidney is made up of about 1 million nephrons, which are the working units of the kidneys, removing wastes and extra fluids from the blood. [NIH] Nephropathy: Disease of the kidneys. [EU] Nephrosis: Descriptive histopathologic term for renal disease without an inflammatory component. [NIH] Nephrotic: Pertaining to, resembling, or caused by nephrosis. [EU] Nephrotic Syndrome: Clinical association of heavy proteinuria, hypoalbuminemia, and generalized edema. [NIH] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nerve Endings: Specialized terminations of peripheral neurons. Nerve endings include neuroeffector junction(s) by which neurons activate target organs and sensory receptors which transduce information from the various sensory modalities and send it centrally in the nervous system. Presynaptic nerve endings are presynaptic terminals. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Networks: Pertaining to a nerve or to the nerves, a meshlike structure of interlocking fibers or strands. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neuralgia: Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve. [NIH] Neuroeffector Junction: The synapse between a neuron (presynaptic) and an effector cell other than another neuron (postsynaptic). Neuroeffector junctions include synapses onto muscles and onto secretory cells. [NIH] Neuroendocrine: Having to do with the interactions between the nervous system and the endocrine system. Describes certain cells that release hormones into the blood in response to stimulation of the nervous system. [NIH] Neurogenic: Loss of bladder control caused by damage to the nerves controlling the bladder. [NIH] Neurologic: Having to do with nerves or the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Diseases: A general term encompassing lower motor neuron disease; peripheral nervous system diseases; and certain muscular diseases. Manifestations include muscle weakness; fasciculation; muscle atrophy; spasm; myokymia; muscle hypertonia, myalgias, and musclehypotonia. [NIH] Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuromuscular Junction Diseases: Conditions characterized by impaired transmission of
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impulses at the neuromuscular junction. This may result from disorders that affect receptor function, pre- or postsynaptic membrane function, or acetylcholinesteraseactivity. The majority of diseases in this category are associated with autoimmune, toxic, or inherited conditions. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neuropeptide: A member of a class of protein-like molecules made in the brain. Neuropeptides consist of short chains of amino acids, with some functioning as neurotransmitters and some functioning as hormones. [NIH] Neurophysiology: The scientific discipline concerned with the physiology of the nervous system. [NIH] Neuropsychological Tests: Tests designed to assess neurological function associated with certain behaviors. They are used in diagnosing brain dysfunction or damage and central nervous system disorders or injury. [NIH] Neurosecretory Systems: A system of neurons that has the specialized function to produce and secrete hormones, and that constitutes, in whole or in part, an endocrine organ or system. [NIH] Neurosurgeon: A doctor who specializes in surgery on the brain, spine, and other parts of the nervous system. [NIH] Neurotensin: A biologically active tridecapeptide isolated from the hypothalamus. It has been shown to induce hypotension in the rat, to stimulate contraction of guinea pig ileum and rat uterus, and to cause relaxation of rat duodenum. There is also evidence that it acts as both a peripheral and a central nervous system neurotransmitter. [NIH] Neurotic: 1. Pertaining to or characterized by neurosis. 2. A person affected with a neurosis. [EU]
Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutrophil: A type of white blood cell. [NIH] Nicardipine: 1,4-Dihydro-2,6-dimethyl-4-(3-nitrophenyl) methyl 2(methyl(phenylmethyl)amino)-3,5-pyridinecarboxylic acid ethyl ester. A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents. [NIH]
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Nicotine: Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke. [NIH] Nicotinic Agonists: Drugs that bind to and activate nicotinic cholinergic receptors (receptors, nicotinic). Nicotinic agonists act at postganglionic nicotinic receptors, at neuroeffector junctions in the peripheral nervous system, and at nicotinic receptors in the central nervous system. Agents that function as neuromuscular depolarizing blocking agents are included here because they activate nicotinic receptors, although they are used clinically to block nicotinic transmission. [NIH] Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful antianginal agent that also lowers blood pressure. The use of nifedipine as a tocolytic is being investigated. [NIH] Nisoldipine: 1,4-Dihydro-2,6-dimethyl-4 (2-nitrophenyl)-3,5-pyridinedicarboxylic acid methyl 2-methylpropyl ester. Nisoldipine is a dihydropyridine calcium channel antagonist that acts as a potent arterial vasodilator and antihypertensive agent. It is also effective in patients with cardiac failure and angina. [NIH] Nitrendipine: Ethyl methyl 2,4-dihydro-2,6-dimethyl-4(3-nitrophenyl)-3,5pyridinedicarboxylate. A calcium channel blocker with marked vasodilator action. It is an effective antihypertensive agent and differs from other calcium channel blockers in that it does not reduce glomerular filtration rate and is mildly natriuretic, rather than sodium retentive. [NIH] Nitric acid: A toxic, corrosive, colorless liquid used to make fertilizers, dyes, explosives, and other chemicals. [NIH] Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]
Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Nitroglycerin: A highly volatile organic nitrate that acts as a dilator of arterial and venous smooth muscle and is used in the treatment of angina. It provides relief through improvement of the balance between myocardial oxygen supply and demand. Although total coronary blood flow is not increased, there is redistribution of blood flow in the heart when partial occlusion of coronary circulation is effected. [NIH] Nitroprusside: (OC-6-22)-Pentakis(cyano-C)nitrosoferrate(2-). A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins. [NIH] Nonmalignant: Not cancerous. [NIH] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used
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pharmacologically as a sympathomimetic. [NIH] Normotensive: 1. Characterized by normal tone, tension, or pressure, as by normal blood pressure. 2. A person with normal blood pressure. [EU] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclear Medicine: A specialty field of radiology concerned with diagnostic, therapeutic, and investigative use of radioactive compounds in a pharmaceutical form. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary bases in the two strains. [NIH] Nucleotidases: A class of enzymes that catalyze the conversion of a nucleotide and water to a nucleoside and orthophosphate. EC 3.1.3.-. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nursing Care: Care given to patients by nursing service personnel. [NIH] Nutritive Value: An indication of the contribution of a food to the nutrient content of the diet. This value depends on the quantity of a food which is digested and absorbed and the amounts of the essential nutrients (protein, fat, carbohydrate, minerals, vitamins) which it contains. This value can be affected by soil and growing conditions, handling and storage, and processing. [NIH] Occult: Obscure; concealed from observation, difficult to understand. [EU] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Ocular Hypertension: A condition in which the intraocular pressure is elevated above normal and which may lead to glaucoma. [NIH] Oculi: Globe or ball of the eye. [NIH] Oculomotor: Cranial nerve III. It originate from the lower ventral surface of the midbrain and is classified as a motor nerve. [NIH] Oculomotor Nerve: The 3d cranial nerve. The oculomotor nerve sends motor fibers to the levator muscles of the eyelid and to the superior rectus, inferior rectus, and inferior oblique muscles of the eye. It also sends parasympathetic efferents (via the ciliary ganglion) to the muscles controlling pupillary constriction and accommodation. The motor fibers originate in the oculomotor nuclei of the midbrain. [NIH] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Odour: A volatile emanation that is perceived by the sense of smell. [EU]
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Oedema: The presence of abnormally large amounts of fluid in the intercellular tissue spaces of the body; usually applied to demonstrable accumulation of excessive fluid in the subcutaneous tissues. Edema may be localized, due to venous or lymphatic obstruction or to increased vascular permeability, or it may be systemic due to heart failure or renal disease. Collections of edema fluid are designated according to the site, e.g. ascites (peritoneal cavity), hydrothorax (pleural cavity), and hydropericardium (pericardial sac). Massive generalized edema is called anasarca. [EU] Oliguria: Clinical manifestation of the urinary system consisting of a decrease in the amount of urine secreted. [NIH] Omega-3 fatty acid: A type of fat obtained in the diet and involved in immunity. [NIH] Omentum: A fold of the peritoneum (the thin tissue that lines the abdomen) that surrounds the stomach and other organs in the abdomen. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Oocytes: Female germ cells in stages between the prophase of the first maturation division and the completion of the second maturation division. [NIH] Oophorectomy: Surgery to remove one or both ovaries. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Open Reading Frames: Reading frames where successive nucleotide triplets can be read as codons specifying amino acids and where the sequence of these triplets is not interrupted by stop codons. [NIH] Operon: The genetic unit consisting of a feedback system under the control of an operator gene, in which a structural gene transcribes its message in the form of mRNA upon blockade of a repressor produced by a regulator gene. Included here is the attenuator site of bacterial operons where transcription termination is regulated. [NIH] Ophthalmic: Pertaining to the eye. [EU] Opiate: A remedy containing or derived from opium; also any drug that induces sleep. [EU] Opioid Peptides: The endogenous peptides with opiate-like activity. The three major classes currently recognized are the enkephalins, the dynorphins, and the endorphins. Each of these families derives from different precursors, proenkephalin, prodynorphin, and proopiomelanocortin, respectively. There are also at least three classes of opioid receptors, but the peptide families do not map to the receptors in a simple way. [NIH] Opium: The air-dried exudate from the unripe seed capsule of the opium poppy, Papaver somniferum, or its variant, P. album. It contains a number of alkaloids, but only a few morphine, codeine, and papaverine - have clinical significance. Opium has been used as an analgesic, antitussive, antidiarrheal, and antispasmodic. [NIH] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes. [NIH]
Optic disc: The circular area (disc) where the optic nerve connects to the retina. [NIH]
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Optic Disk: The portion of the optic nerve seen in the fundus with the ophthalmoscope. It is formed by the meeting of all the retinal ganglion cell axons as they enter the optic nerve. [NIH]
Optic Nerve: The 2nd cranial nerve. The optic nerve conveys visual information from the retina to the brain. The nerve carries the axons of the retinal ganglion cells which sort at the optic chiasm and continue via the optic tracts to the brain. The largest projection is to the lateral geniculate nuclei; other important targets include the superior colliculi and the suprachiasmatic nuclei. Though known as the second cranial nerve, it is considered part of the central nervous system. [NIH] Optic Nerve Diseases: Conditions which produce injury or dysfunction of the second cranial or optic nerve, which is generally considered a component of the central nervous system. Damage to optic nerve fibers may occur at or near their origin in the retina, at the optic disk, or in the nerve, optic chiasm, optic tract, or lateral geniculate nuclei. Clinical manifestations may include decreased visual acuity and contrast sensitivity, impaired color vision, and an afferent pupillary defect. [NIH] Optic nerve head: The circular area (disc) where the optic nerve connects to the retina. [NIH] Organ Culture: The growth in aseptic culture of plant organs such as roots or shoots, beginning with organ primordia or segments and maintaining the characteristics of the organ. [NIH] Organ Transplantation: Transference of an organ between individuals of the same species or between individuals of different species. [NIH] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Orgasm: The crisis of sexual excitement in either humans or animals. [NIH] Orlistat: A lipase inhibitor used for weight loss. Lipase is an enzyme found in the bowel that assists in lipid absorption by the body. Orlistat blocks this enzyme, reducing the amount of fat the body absorbs by about 30 percent. It is known colloquially as a "fat blocker." Because more oily fat is left in the bowel to be excreted, Orlistat can cause an oily anal leakage and fecal incontinence. Orlistat may not be suitable for people with bowel conditions such as irritable bowel syndrome or Crohn's disease. [NIH] Orthostatic: Pertaining to or caused by standing erect. [EU] Osmolality: The concentration of osmotically active particles in solution expressed in terms of osmoles of solute per kilogram of solvent. The osmolality is directly proportional to the colligative properties of solutions; osmotic pressure, boiling point elevation, freezing point depression, and vapour pressure lowering. [EU] Osmoles: The standard unit of osmotic pressure. [NIH] Osmosis: Tendency of fluids (e.g., water) to move from the less concentrated to the more concentrated side of a semipermeable membrane. [NIH] Osmotic: Pertaining to or of the nature of osmosis (= the passage of pure solvent from a solution of lesser to one of greater solute concentration when the two solutions are separated by a membrane which selectively prevents the passage of solute molecules, but is permeable to the solvent). [EU] Ossification: The formation of bone or of a bony substance; the conversion of fibrous tissue or of cartilage into bone or a bony substance. [EU] Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but
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from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans. [NIH] Osteodystrophy: Defective bone formation. [EU] Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Ouabain: A cardioactive glycoside consisting of rhamnose and ouabagenin, obtained from the seeds of Strophanthus gratus and other plants of the Apocynaceae; used like digitalis. It is commonly used in cell biological studies as an inhibitor of the NA(+)-K(+)-exchanging atpase. [NIH] Outpatient: A patient who is not an inmate of a hospital but receives diagnosis or treatment in a clinic or dispensary connected with the hospital. [NIH] Ovariectomy: The surgical removal of one or both ovaries. [NIH] Ovaries: The pair of female reproductive glands in which the ova, or eggs, are formed. The ovaries are located in the pelvis, one on each side of the uterus. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Overexpress: An excess of a particular protein on the surface of a cell. [NIH] Overweight: An excess of body weight but not necessarily body fat; a body mass index of 25 to 29.9 kg/m2. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxalate: A chemical that combines with calcium in urine to form the most common type of kidney stone (calcium oxalate stone). [NIH] Oxalic Acid: A strong dicarboxylic acid occurring in many plants and vegetables. It is produced in the body by metabolism of glyoxylic acid or ascorbic acid. It is not metabolized but excreted in the urine. It is used as an analytical reagent and general reducing agent. [NIH] Oxidants: Oxidizing agents or electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (oxidation-reduction). In vivo, it appears that phagocyte-generated oxidants function as tumor promoters or cocarcinogens rather than as complete carcinogens perhaps because of the high levels of endogenous antioxidant defenses. It is also thought that oxidative damage in joints may trigger the autoimmune response that characterizes the persistence of the rheumatoid disease process. [NIH]
Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471). [NIH] Oxidative metabolism: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as aerobic respiration, cell respiration, or aerobic metabolism. [NIH]
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Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oxides: Binary compounds of oxygen containing the anion O(2-). The anion combines with metals to form alkaline oxides and non-metals to form acidic oxides. [NIH] Oximetry: The determination of oxygen-hemoglobin saturation of blood either by withdrawing a sample and passing it through a classical photoelectric oximeter or by electrodes attached to some translucent part of the body like finger, earlobe, or skin fold. It includes non-invasive oxygen monitoring by pulse oximetry. [NIH] Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH] Oxygenase: Enzyme which breaks down heme, the iron-containing oxygen-carrying constituent of the red blood cells. [NIH] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 oxygenation the process of supplying, treating, or mixing with oxygen. [EU] Oxygenator: An apparatus by which oxygen is introduced into the blood during circulation outside the body, as during open heart surgery. [NIH] Oxytocin: A nonapeptide posterior pituitary hormone that causes uterine contractions and stimulates lactation. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Palsy: Disease of the peripheral nervous system occurring usually after many years of increased lead absorption. [NIH] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic cancer: Cancer of the pancreas, a salivary gland of the abdomen. [NIH] Pancreatitis: Acute or chronic inflammation of the pancreas, which may be asymptomatic or symptomatic, and which is due to autodigestion of a pancreatic tissue by its own enzymes. It is caused most often by alcoholism or biliary tract disease; less commonly it may be associated with hyperlipaemia, hyperparathyroidism, abdominal trauma (accidental or operative injury), vasculitis, or uraemia. [EU] Panic: A state of extreme acute, intense anxiety and unreasoning fear accompanied by disorganization of personality function. [NIH] Papain: A proteolytic enzyme obtained from Carica papaya. It is also the name used for a purified mixture of papain and chymopapain that is used as a topical enzymatic debriding agent. EC 3.4.22.2. [NIH] Papilla: A small nipple-shaped elevation. [NIH] Papilledema: Swelling around the optic disk. [NIH] Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [NIH] Parasitic: Having to do with or being a parasite. A parasite is an animal or a plant that lives on or in an organism of another species and gets at least some of its nutrients from it. [NIH]
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Parathyroid: 1. Situated beside the thyroid gland. 2. One of the parathyroid glands. 3. A sterile preparation of the water-soluble principle(s) of the parathyroid glands, ad-ministered parenterally as an antihypocalcaemic, especially in the treatment of acute hypoparathyroidism with tetany. [EU] Parathyroid Glands: Two small paired endocrine glands in the region of the thyroid gland. They secrete parathyroid hormone and are concerned with the metabolism of calcium and phosphorus. [NIH] Parathyroid hormone: A substance made by the parathyroid gland that helps the body store and use calcium. Also called parathormone, parathyrin, or PTH. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] Parietal: 1. Of or pertaining to the walls of a cavity. 2. Pertaining to or located near the parietal bone, as the parietal lobe. [EU] Parietal Lobe: Upper central part of the cerebral hemisphere. [NIH] Parotid: The space that contains the parotid gland, the facial nerve, the external carotid artery, and the retromandibular vein. [NIH] Paroxetine: A serotonin uptake inhibitor that is effective in the treatment of depression. [NIH]
Paroxysmal: Recurring in paroxysms (= spasms or seizures). [EU] Partial remission: The shrinking, but not complete disappearance, of a tumor in response to therapy. Also called partial response. [NIH] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Patent ductus arteriosus: Abnormal persistence of the opening in the arterial duct that connects the pulmonary artery to the descending aorta; this opening normally closes within 24 hours of birth. [NIH] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]
Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Care Management: Generating, planning, organizing, and administering medical and nursing care and services for patients. [NIH] Patient Compliance: Voluntary cooperation of the patient in following a prescribed regimen. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
Patient Satisfaction: The degree to which the individual regards the health care service or product or the manner in which it is delivered by the provider as useful, effective, or beneficial. [NIH]
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Pediatrics: A medical specialty concerned with maintaining health and providing medical care to children from birth to adolescence. [NIH] Pedigree: A record of one's ancestors, offspring, siblings, and their offspring that may be used to determine the pattern of certain genes or disease inheritance within a family. [NIH] Pelvic: Pertaining to the pelvis. [EU] Pelvis: The lower part of the abdomen, located between the hip bones. [NIH] Penicillin: An antibiotic drug used to treat infection. [NIH] Penis: The external reproductive organ of males. It is composed of a mass of erectile tissue enclosed in three cylindrical fibrous compartments. Two of the three compartments, the corpus cavernosa, are placed side-by-side along the upper part of the organ. The third compartment below, the corpus spongiosum, houses the urethra. [NIH] Pepsin: An enzyme made in the stomach that breaks down proteins. [NIH] Pepsinogen C: This is one of the 2 related pepsinogen systems in humans. It is found in prostate and seminal fluid whereas pepsinogen A is not. [NIH] Peptic: Pertaining to pepsin or to digestion; related to the action of gastric juices. [EU] Peptic Ulcer: Ulcer that occurs in those portions of the alimentary tract which come into contact with gastric juice containing pepsin and acid. It occurs when the amount of acid and pepsin is sufficient to overcome the gastric mucosal barrier. [NIH] Peptic Ulcer Hemorrhage: Bleeding from a peptic ulcer. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins. [NIH] Peptide Hydrolases: A subclass of enzymes from the hydrolase class that catalyze the hydrolysis of peptide bonds. Exopeptidases and endopeptidases make up the sub-subclasses for this group. EC 3.4. [NIH] Peptide T: N-(N-(N(2)-(N-(N-(N-(N-D-Alanyl L-seryl)-L-threonyl)-L-threonyl) L-threonyl)L-asparaginyl)-L-tyrosyl) L-threonine. Octapeptide sharing sequence homology with HIV envelope protein gp120. It is potentially useful as antiviral agent in AIDS therapy. The core pentapeptide sequence, TTNYT, consisting of amino acids 4-8 in peptide T, is the HIV envelope sequence required for attachment to the CD4 receptor. [NIH] Perception: The ability quickly and accurately to recognize similarities and differences among presented objects, whether these be pairs of words, pairs of number series, or multiple sets of these or other symbols such as geometric figures. [NIH] Perennial: Lasting through the year of for several years. [EU] Perforation: 1. The act of boring or piercing through a part. 2. A hole made through a part or substance. [EU] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Pericarditis: Inflammation of the pericardium. [EU] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]
Pericytes: Smooth muscle cell that wraps around normal blood vessels. [NIH] Perimenopausal: The time of a woman's life when menstrual periods become irregular. Refers to the time near menopause. [NIH]
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Perimetry: Determination of the extent of the visual field for various types and intensities of stimuli. [NIH] Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] Perindopril: An angiotensin-converting enzyme inhibitor. It is used in patients with hypertension and heart failure. [NIH] Perioperative: Around the time of surgery; usually lasts from the time of going into the hospital or doctor's office for surgery until the time the patient goes home. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral Nervous System Diseases: Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves. [NIH] Peripheral Vascular Disease: Disease in the large blood vessels of the arms, legs, and feet. People who have had diabetes for a long time may get this because major blood vessels in their arms, legs, and feet are blocked and these limbs do not receive enough blood. The signs of PVD are aching pains in the arms, legs, and feet (especially when walking) and foot sores that heal slowly. Although people with diabetes cannot always avoid PVD, doctors say they have a better chance of avoiding it if they take good care of their feet, do not smoke, and keep both their blood pressure and diabetes under good control. [NIH] Peripheral vision: Side vision; ability to see objects and movement outside of the direct line of vision. [NIH] Peristalsis: The rippling motion of muscles in the intestine or other tubular organs characterized by the alternate contraction and relaxation of the muscles that propel the contents onward. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneal Cavity: The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen. [NIH] Peritoneal Dialysis: Dialysis fluid being introduced into and removed from the peritoneal cavity as either a continuous or an intermittent procedure. [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Perivascular: Situated around a vessel. [EU] Peroxide: Chemical compound which contains an atom group with two oxygen atoms tied to each other. [NIH] Perspiration: Sweating; the functional secretion of sweat. [EU] Pertussis: An acute, highly contagious infection of the respiratory tract, most frequently affecting young children, usually caused by Bordetella pertussis; a similar illness has been
Dictionary 535
associated with infection by B. parapertussis and B. bronchiseptica. It is characterized by a catarrhal stage, beginning after an incubation period of about two weeks, with slight fever, sneezing, running at the nose, and a dry cough. In a week or two the paroxysmal stage begins, with the characteristic paroxysmal cough, consisting of a deep inspiration, followed by a series of quick, short coughs, continuing until the air is expelled from the lungs; the close of the paroxysm is marked by a long-drawn, shrill, whooping inspiration, due to spasmodic closure of the glottis. This stage lasts three to four weeks, after which the convalescent stage begins, in which paroxysms grow less frequent and less violent, and finally cease. Called also whooping cough. [EU] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Pharmaceutical Preparations: Drugs intended for human or veterinary use, presented in their finished dosage form. Included here are materials used in the preparation and/or formulation of the finished dosage form. [NIH] Pharmacist: A person trained to prepare and distribute medicines and to give information about them. [NIH] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharmacotherapy: A regimen of using appetite suppressant medications to manage obesity by decreasing appetite or increasing the feeling of satiety. These medications decrease appetite by increasing serotonin or catecholamine—two brain chemicals that affect mood and appetite. [NIH] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phenoxybenzamine: An alpha-adrenergic anatagonist with long duration of action. It has been used to treat hypertension and as a peripheral vasodilator. [NIH] Phenyl: Ingredient used in cold and flu remedies. [NIH] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phenylephrine: An alpha-adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent. [NIH] Phenytoin: An anticonvulsant that is used in a wide variety of seizures. It is also an antiarrhythmic and a muscle relaxant. The mechanism of therapeutic action is not clear, although several cellular actions have been described including effects on ion channels, active transport, and general membrane stabilization. The mechanism of its muscle relaxant effect appears to involve a reduction in the sensitivity of muscle spindles to stretch. Phenytoin has been proposed for several other therapeutic uses, but its use has been limited by its many adverse effects and interactions with other drugs. [NIH] Phosphates: Inorganic salts of phosphoric acid. [NIH]
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Phosphodiesterase: Effector enzyme that regulates the levels of a second messenger, the cyclic GMP. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphoric Monoester Hydrolases: A group of hydrolases which catalyze the hydrolysis of monophosphoric esters with the production of one mole of orthophosphate. EC 3.1.3. [NIH] Phosphorous: Having to do with or containing the element phosphorus. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylate: Attached to a phosphate group. [NIH] Phosphorylated: Attached to a phosphate group. [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photocoagulation: Using a special strong beam of light (laser) to seal off bleeding blood vessels such as in the eye. The laser can also burn away blood vessels that should not have grown in the eye. This is the main treatment for diabetic retinopathy. [NIH] Phrenic Nerve: The motor nerve of the diaphragm. The phrenic nerve fibers originate in the cervical spinal column (mostly C4) and travel through the cervical plexus to the diaphragm. [NIH]
Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physical Therapy: The restoration of function and the prevention of disability following disease or injury with the use of light, heat, cold, water, electricity, ultrasound, and exercise. [NIH]
Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]
Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Physostigmine: A cholinesterase inhibitor that is rapidly absorbed through membranes. It can be applied topically to the conjunctiva. It also can cross the blood-brain barrier and is used when central nervous system effects are desired, as in the treatment of severe anticholinergic toxicity. [NIH] Pigmentation: Coloration or discoloration of a part by a pigment. [NIH] Pigments: Any normal or abnormal coloring matter in plants, animals, or micro-organisms. [NIH]
Pilocarpine: A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma. [NIH] Piloerection: Involuntary erection or bristling of hairs. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH]
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Piroxicam: 4-Hydroxy-2-methyl-N-2-pyridyl-2H-1,2-benzothiazine-3-carboxamide 1,1dioxide. A non-steroidal anti-inflammatory agent that is well established in the treatment of rheumatoid arthritis and osteoarthritis. Its usefulness has also been demonstrated in the treatment of musculoskeletal disorders, dysmenorrhea, and postoperative pain. Its long half-life enables it to be administered once daily. The drug has also been shown to be effective if administered rectally. Gastrointestinal complaints are the most frequently reported side effects. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Plasmid: An autonomously replicating, extra-chromosomal DNA molecule found in many bacteria. Plasmids are widely used as carriers of cloned genes. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH] Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Plasticity: In an individual or a population, the capacity for adaptation: a) through gene changes (genetic plasticity) or b) through internal physiological modifications in response to changes of environment (physiological plasticity). [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to
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the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]
Plethysmography: Recording of change in the size of a part as modified by the circulation in it. [NIH] Pleural: A circumscribed area of hyaline whorled fibrous tissue which appears on the surface of the parietal pleura, on the fibrous part of the diaphragm or on the pleura in the interlobar fissures. [NIH] Pleural cavity: A space enclosed by the pleura (thin tissue covering the lungs and lining the interior wall of the chest cavity). It is bound by thin membranes. [NIH] Pneumonia: Inflammation of the lungs. [NIH] Pneumothorax: Accumulation of air or gas in the space between the lung and chest wall, resulting in partial or complete collapse of the lung. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Polyarteritis Nodosa: A form of necrotizing vasculitis involving small- and medium-sized arteries. The signs and symptoms result from infarction and scarring of the affected organ system. [NIH] Polycystic: An inherited disorder characterized by many grape-like clusters of fluid-filled cysts that make both kidneys larger over time. These cysts take over and destroy working kidney tissue. PKD may cause chronic renal failure and end-stage renal disease. [NIH] Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polyunsaturated fat: An unsaturated fat found in greatest amounts in foods derived from plants, including safflower, sunflower, corn, and soybean oils. [NIH] Pons: The part of the central nervous system lying between the medulla oblongata and the mesencephalon, ventral to the cerebellum, and consisting of a pars dorsalis and a pars ventralis. [NIH] Porphyria: A group of disorders characterized by the excessive production of porphyrins or their precursors that arises from abnormalities in the regulation of the porphyrin-heme pathway. The porphyrias are usually divided into three broad groups, erythropoietic, hepatic, and erythrohepatic, according to the major sites of abnormal porphyrin synthesis. [NIH]
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Porphyrins: A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin. [NIH] Portacaval: Surgical creation of an anastomosis between the portal and caval veins. [NIH] Portal Hypertension: High blood pressure in the portal vein. This vein carries blood into the liver. Portal hypertension is caused by a blood clot. This is a common complication of cirrhosis. [NIH] Portal Pressure: The venous pressure measured in the portal vein. [NIH] Portal System: A system of vessels in which blood, after passing through one capillary bed, is conveyed through a second set of capillaries before it returns to the systemic circulation. It pertains especially to the hepatic portal system. [NIH] Portal Vein: A short thick vein formed by union of the superior mesenteric vein and the splenic vein. [NIH] Portosystemic Shunt: An operation to create an opening between the portal vein and other veins around the liver. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Posterior chamber: The space between the back of the iris and the front face of the vitreous; filled with aqueous fluid. [NIH] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postoperative: After surgery. [NIH] Postoperative Complications: Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery. [NIH] Postprandial: Occurring after dinner, or after a meal; postcibal. [EU] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Post-synaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Postural: Pertaining to posture or position. [EU] Potassium: An element that is in the alkali group of metals. It has an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte and it plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance. [NIH] Potassium Channels: Cell membrane glycoproteins selective for potassium ions. [NIH] Potentiate: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiating: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis,
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therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Pravastatin: An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (hydroxymethylglutaryl CoA reductases). [NIH] Prazosin: A selective adrenergic alpha-1 antagonist used in the treatment of heart failure, hypertension, pheochromocytoma, Raynaud's syndrome, prostatic hypertrophy, and urinary retention. [NIH] Precipitating Factors: Factors associated with the definitive onset of a disease, illness, accident, behavioral response, or course of action. Usually one factor is more important or more obviously recognizable than others, if several are involved, and one may often be regarded as "necessary". Examples include exposure to specific disease; amount or level of an infectious organism, drug, or noxious agent, etc. [NIH] Preclinical: Before a disease becomes clinically recognizable. [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predictive factor: A situation or condition that may increase a person's risk of developing a certain disease or disorder. [NIH] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Preeclampsia: A toxaemia of late pregnancy characterized by hypertension, edema, and proteinuria, when convulsions and coma are associated, it is called eclampsia. [EU] Pre-Eclampsia: Development of hypertension with proteinuria, edema, or both, due to pregnancy or the influence of a recent pregnancy. It occurs after the 20th week of gestation, but it may develop before this time in the presence of trophoblastic disease. [NIH] Pre-eclamptic: A syndrome characterized by hypertension, albuminuria, and generalized oedema, occurring only in pregnancy. [NIH] Prekallikrein: A plasma protein which is the precursor of kallikrein. Plasma that is deficient in prekallikrein has been found to be abnormal in thromboplastin formation, kinin generation, evolution of a permeability globulin, and plasmin formation. The absence of prekallikrein in plasma leads to Fletcher factor deficiency, a congenital disease. [NIH] Premenopausal: Refers to the time before menopause. Menopause is the time of life when a women's menstrual periods stop permanently; also called "change of life." [NIH] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Prenatal Care: Care provided the pregnant woman in order to prevent complications, and decrease the incidence of maternal and prenatal mortality. [NIH] Preoperative: Preceding an operation. [EU] Pressoreceptors: Receptors in the vascular system, particularly the aorta and carotid sinus, which are sensitive to stretch of the vessel walls. [NIH] Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Presynaptic Terminals: The distal terminations of axons which are specialized for the release of neurotransmitters. Also included are varicosities along the course of axons which have similar specializations and also release transmitters. Presynaptic terminals in both the
Dictionary 541
central and peripheral nervous systems are included. [NIH] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Priapism: Persistent abnormal erection of the penis, usually without sexual desire, and accompanied by pain and tenderness. It is seen in diseases and injuries of the spinal cord, and may be caused by vesical calculus and certain injuries to the penis. [EU] Primary Prevention: Prevention of disease or mental disorders in susceptible individuals or populations through promotion of health, including mental health, and specific protection, as in immunization, as distinguished from the prevention of complications or after-effects of existing disease. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Problem-Based Learning: Instructional use of examples or cases to teach using problemsolving skills and critical thinking. [NIH] Procainamide: A derivative of procaine with less CNS action. [NIH] Procaine: A local anesthetic of the ester type that has a slow onset and a short duration of action. It is mainly used for infiltration anesthesia, peripheral nerve block, and spinal block. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1016). [NIH] Prodrug: A substance that gives rise to a pharmacologically active metabolite, although not itself active (i. e. an inactive precursor). [NIH] Progeny: The offspring produced in any generation. [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Prognostic factor: A situation or condition, or a characteristic of a patient, that can be used to estimate the chance of recovery from a disease, or the chance of the disease recurring (coming back). [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Progressive disease: Cancer that is increasing in scope or severity. [NIH] Proinsulin: The substance made first in the pancreas that is then made into insulin. When insulin is purified from the pancreas of pork or beef, all the proinsulin is not fully removed. When some people use these insulins, the proinsulin can cause the body to react with a rash, to resist the insulin, or even to make dents or lumps in the skin at the place where the insulin is injected. The purified insulins have less proinsulin and other impurities than the other types of insulins. [NIH] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Prolactin: Pituitary lactogenic hormone. A polypeptide hormone with a molecular weight of about 23,000. It is essential in the induction of lactation in mammals at parturition and is synergistic with estrogen. The hormone also brings about the release of progesterone from lutein cells, which renders the uterine mucosa suited for the embedding of the ovum should
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fertilization occur. [NIH] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prone: Having the front portion of the body downwards. [NIH] Propanolol: Beta blocker. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Proportional: Being in proportion : corresponding in size, degree, or intensity, having the same or a constant ratio; of, relating to, or used in determining proportions. [EU] Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol is used in the treatment or prevention of many disorders including acute myocardial infarction, arrhythmias, angina pectoris, hypertension, hypertensive emergencies, hyperthyroidism, migraine, pheochromocytoma, menopause, and anxiety. [NIH] Prospective Studies: Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandin Endoperoxides: Precursors in the biosynthesis of prostaglandins and thromboxanes from arachidonic acid. They are physiologically active compounds, having effect on vascular and airway smooth muscles, platelet aggregation, etc. [NIH] Prostaglandin-Endoperoxide Synthase: An enzyme complex that catalyzes the formation of prostaglandins from the appropriate unsaturated fatty acid, molecular oxygen, and a reduced acceptor. EC 1.14.99.1. [NIH]
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Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Prostaglandins D: Physiologically active prostaglandins found in many tissues and organs. They show pressor activity, are mediators of inflammation, and have potential antithrombotic effects. [NIH] Prostaglandins F: (9 alpha,11 alpha,13E,15S)-9,11,15-Trihydroxyprost-13-en-1-oic acid (PGF(1 alpha)); (5Z,9 alpha,11,alpha,13E,15S)-9,11,15-trihydroxyprosta-5,13-dien-1-oic acid (PGF(2 alpha)); (5Z,9 alpha,11 alpha,13E,15S,17Z)-9,11,15-trihydroxyprosta-5,13,17-trien-1oic acid (PGF(3 alpha)). A family of prostaglandins that includes three of the six naturally occurring prostaglandins. All naturally occurring PGF have an alpha configuration at the 9carbon position. They stimulate uterine and bronchial smooth muscle and are often used as oxytocics. [NIH] Prostaglandins G: A group of physiologically active prostaglandin endoperoxides. They are precursors in the biosynthesis of prostaglandins and thromboxanes. Most frequently encountered member of this group is the prostaglandin G2. [NIH] Prostaglandins H: A group of physiologically active prostaglandin endoperoxides. They are precursors in the biosynthesis of prostaglandins and thromboxanes. The most frequently encountered member of this group is the prostaglandin H2. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protective Agents: Synthetic or natural substances which are given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent. [NIH]
Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific proteinbinding measures are often used as assays in diagnostic assessments. [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein. EC 2.7.1.37. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteoglycans: Glycoproteins which have a very high polysaccharide content. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that
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promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Prothrombin: A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia. [NIH]
Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Pseudohypoaldosteronism: A hereditary disorder characterized by salt wasting and growth retardation, presenting in infancy as high levels of urinary sodium despite hyponatremia, hyperkalemia, hyperreninemia, and elevated aldosterone levels. The mode of inheritance is probably autosomal dominant, affecting electrolyte secretion in the kidney tubule. [NIH] Pseudotumor Cerebri: A condition marked by raised intracranial pressure and characterized clinically by headaches; nausea; papilledema, peripheral constriction of the visual fields, transient visual obscurations, and pulsatile tinnitus. Obesity is frequently associated with this condition, which primarily affects women between 20 and 44 years of age. Chronic papilledema may lead to optic nerve injury (optic nerve diseases) and visual loss (blindness). [NIH] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychoactive: Those drugs which alter sensation, mood, consciousness or other psychological or behavioral functions. [NIH] Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Psychomotor: Pertaining to motor effects of cerebral or psychic activity. [EU] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Pulmonary: Relating to the lungs. [NIH] Pulmonary Alveoli: Small polyhedral outpouchings along the walls of the alveolar sacs, alveolar ducts and terminal bronchioles through the walls of which gas exchange between alveolar air and pulmonary capillary blood takes place. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulmonary Circulation: The circulation of blood through the lungs. [NIH] Pulmonary Edema: An accumulation of an excessive amount of watery fluid in the lungs, may be caused by acute exposure to dangerous concentrations of irritant gasses. [NIH]
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Pulmonary hypertension: Abnormally high blood pressure in the arteries of the lungs. [NIH] Pulmonary Veins: The veins that return the oxygenated blood from the lungs to the left atrium of the heart. [NIH] Pulmonary Ventilation: The total volume of gas per minute inspired or expired measured in liters per minute. [NIH] Pulsation: A throb or rhythmical beat, as of the heart. [EU] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Pupil: The aperture in the iris through which light passes. [NIH] Purified Insulins: Insulins with much less of the impure proinsulin. It is thought that the use of purified insulins may help avoid or reduce some of the problems of people with diabetes such as allergic reactions. [NIH] Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Purpura: Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. [NIH] Pyelonephritis: Inflammation of the kidney and its pelvis, beginning in the interstitium and rapidly extending to involve the tubules, glomeruli, and blood vessels; due to bacterial infection. [EU] Pyridoxal: 3-Hydroxy-5-(hydroxymethyl)-2-methyl-4- pyridinecarboxaldehyde. [NIH] Pyridoxal Phosphate: 3-Hydroxy-2-methyl-5-((phosphonooxy)methyl)-4pyridinecarboxaldehyde. An enzyme co-factor vitamin. [NIH] Pyrimidines: A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (cytosine, thymine, and uracil) and form the basic structure of the barbiturates. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Quaternary: 1. Fourth in order. 2. Containing four elements or groups. [EU] Quiescent: Marked by a state of inactivity or repose. [EU] Quinidine: An optical isomer of quinine, extracted from the bark of the Cinchona tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular action potential, and decreases automaticity. Quinidine also blocks muscarinic and alphaadrenergic neurotransmission. [NIH] Quinine: An alkaloid derived from the bark of the cinchona tree. It is used as an antimalarial drug, and is the active ingredient in extracts of the cinchona that have been used for that purpose since before 1633. Quinine is also a mild antipyretic and analgesic and has been used in common cold preparations for that purpose. It was used commonly and as a bitter and flavoring agent, and is still useful for the treatment of babesiosis. Quinine is also useful in some muscular disorders, especially nocturnal leg cramps and myotonia congenita, because of its direct effects on muscle membrane and sodium channels. The mechanisms of its antimalarial effects are not well understood. [NIH] Race: A population within a species which exhibits general similarities within itself, but is
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both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Racemic: Optically inactive but resolvable in the way of all racemic compounds. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radioactive: Giving off radiation. [NIH] Radiography: Examination of any part of the body for diagnostic purposes by means of roentgen rays, recording the image on a sensitized surface (such as photographic film). [NIH] Radioimmunoassay: Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Nonimmunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation. [NIH] Radioimmunotherapy: Radiotherapy where cytotoxic radionuclides are linked to antibodies in order to deliver toxins directly to tumor targets. Therapy with targeted radiation rather than antibody-targeted toxins (immunotoxins) has the advantage that adjacent tumor cells, which lack the appropriate antigenic determinants, can be destroyed by radiation cross-fire. Radioimmunotherapy is sometimes called targeted radiotherapy, but this latter term can also refer to radionuclides linked to non-immune molecules (radiotherapy). [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH] Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [NIH] Ramipril: A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat. [NIH] Random Allocation: A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects. [NIH] Randomization: Also called random allocation. Is allocation of individuals to groups, e.g., for experimental and control regimens, by chance. Within the limits of chance variation, random allocation should make the control and experimental groups similar at the start of an investigation and ensure that personal judgment and prejudices of the investigator do not influence allocation. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that
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the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Randomized Controlled Trials: Clinical trials that involve at least one test treatment and one control treatment, concurrent enrollment and follow-up of the test- and control-treated groups, and in which the treatments to be administered are selected by a random process, such as the use of a random-numbers table. Treatment allocations using coin flips, odd-even numbers, patient social security numbers, days of the week, medical record numbers, or other such pseudo- or quasi-random processes, are not truly randomized and trials employing any of these techniques for patient assignment are designated simply controlled clinical trials. [NIH] Rarefaction: The reduction of the density of a substance; the attenuation of a gas. [NIH] Reaction Time: The time from the onset of a stimulus until the organism responds. [NIH] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Receptors, Serotonin: Cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Recovery of Function: A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma. [NIH] Rectal: By or having to do with the rectum. The rectum is the last 8 to 10 inches of the large intestine and ends at the anus. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflex: An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord. [NIH]
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Reflux: The term used when liquid backs up into the esophagus from the stomach. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractory: Not readily yielding to treatment. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regression Analysis: Procedures for finding the mathematical function which best describes the relationship between a dependent variable and one or more independent variables. In linear regression (see linear models) the relationship is constrained to be a straight line and least-squares analysis is used to determine the best fit. In logistic regression (see logistic models) the dependent variable is qualitative rather than continuously variable and likelihood functions are used to find the best relationship. In multiple regression the dependent variable is considered to depend on more than a single independent variable. [NIH]
Regurgitation: A backward flowing, as the casting up of undigested food, or the backward flowing of blood into the heart, or between the chambers of the heart when a valve is incompetent. [EU] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Renal Artery: A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters. [NIH] Renal Circulation: The circulation of the blood through the vessels of the kidney. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Renal pelvis: The area at the center of the kidney. Urine collects here and is funneled into the ureter, the tube that connects the kidney to the bladder. [NIH] Renal Plasma Flow: The amount of plasma that perfuses the kidneys per unit time, approximately 10% greater than effective renal plasma flow (renal plasma flow, effective). It should be differentiated from the renal blood flow (RBF) which refers to the total volume of blood flowing through the renal vasculature, while the renal plasma flow refers to the rate of plasma flow (RPF). [NIH] Renal tubular: A defect in the kidneys that hinders their normal excretion of acids. Failure to excrete acids can lead to weak bones, kidney stones, and poor growth in children. [NIH] Renin: An enzyme which is secreted by the kidney and is formed from prorenin in plasma and kidney. The enzyme cleaves the Leu-Leu bond in angiotensinogen to generate angiotensin I. EC 3.4.23.15. (Formerly EC 3.4.99.19). [NIH] Renin-Angiotensin System: A system consisting of renin, angiotensin-converting enzyme, and angiotensin II. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an
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alpha-2 globulin produced by the liver, forming angiotensin I. The converting enzyme contained in the lung acts on angiotensin I in the plasma converting it to angiotensin II, the most powerful directly pressor substance known. It causes contraction of the arteriolar smooth muscle and has other indirect actions mediated through the adrenal cortex. [NIH] Renovascular: Of or pertaining to the blood vessels of the kidneys. [EU] Reperfusion: Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing reperfusion injury. [NIH] Reperfusion Injury: Functional, metabolic, or structural changes, including necrosis, in ischemic tissues thought to result from reperfusion to ischemic areas of the tissue. The most common instance is myocardial reperfusion injury. [NIH] Repressor: Any of the specific allosteric protein molecules, products of regulator genes, which bind to the operator of operons and prevent RNA polymerase from proceeding into the operon to transcribe messenger RNA. [NIH] Reproductive cells: Egg and sperm cells. Each mature reproductive cell carries a single set of 23 chromosomes. [NIH] Research Design: A plan for collecting and utilizing data so that desired information can be obtained with sufficient precision or so that an hypothesis can be tested properly. [NIH] Research Support: Financial support of research activities. [NIH] Resorption: The loss of substance through physiologic or pathologic means, such as loss of dentin and cementum of a tooth, or of the alveolar process of the mandible or maxilla. [EU] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respiratory distress syndrome: A lung disease that occurs primarily in premature infants; the newborn must struggle for each breath and blueing of its skin reflects the baby's inability to get enough oxygen. [NIH] Respiratory Paralysis: Complete or severe weakness of the muscles of respiration. This condition may be associated with motor neuron diseases; peripheral nerve disorders; neuromuscular junction diseases; spinal cord diseases; injury to the phrenic nerve; and other disorders. [NIH] Respiratory Physiology: Functions and activities of the respiratory tract as a whole or of any of its parts. [NIH] Respiratory System: The tubular and cavernous organs and structures, by means of which pulmonary ventilation and gas exchange between ambient air and the blood are brought about. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Resuscitation: The restoration to life or consciousness of one apparently dead; it includes such measures as artificial respiration and cardiac massage. [EU] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic
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nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinae: A congenital notch or cleft of the retina, usually located inferiorly. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinal Ganglion Cells: Cells of the innermost nuclear layer of the retina, the ganglion cell layer, which project axons through the optic nerve to the brain. They are quite variable in size and in the shapes of their dendritic arbors, which are generally confined to the inner plexiform layer. [NIH] Retinal Hemorrhage: Bleeding from the vessels of the retina. [NIH] Retinal Neovascularization: Formation of new blood vessels originating from the retinal veins and extending along the inner (vitreal) surface of the retina. [NIH] Retinal Vein: Central retinal vein and its tributaries. It runs a short course within the optic nerve and then leaves and empties into the superior ophthalmic vein or cavernous sinus. [NIH]
Retinoblastoma: An eye cancer that most often occurs in children younger than 5 years. It occurs in hereditary and nonhereditary (sporadic) forms. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retinopathy: 1. Retinitis (= inflammation of the retina). 2. Retinosis (= degenerative, noninflammatory condition of the retina). [EU] Retrograde: 1. Moving backward or against the usual direction of flow. 2. Degenerating, deteriorating, or catabolic. [EU] Retroperitoneal: Having to do with the area outside or behind the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Retrospective: Looking back at events that have already taken place. [NIH] Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Rhamnose: A methylpentose whose L- isomer is found naturally in many plant glycosides and some gram-negative bacterial lipopolysaccharides. [NIH] Rheumatic Diseases: Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH] Rheumatoid: Resembling rheumatism. [EU] Rheumatoid arthritis: A form of arthritis, the cause of which is unknown, although infection, hypersensitivity, hormone imbalance and psychologic stress have been suggested as possible causes. [NIH] Rhodopsin: A photoreceptor protein found in retinal rods. It is a complex formed by the
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binding of retinal, the oxidized form of retinol, to the protein opsin and undergoes a series of complex reactions in response to visible light resulting in the transmission of nerve impulses to the brain. [NIH] Riboflavin: Nutritional factor found in milk, eggs, malted barley, liver, kidney, heart, and leafy vegetables. The richest natural source is yeast. It occurs in the free form only in the retina of the eye, in whey, and in urine; its principal forms in tissues and cells are as FMN and FAD. [NIH] Ribonuclease: RNA-digesting enzyme. [NIH] Ribonucleoside Diphosphate Reductase: An enzyme of the oxidoreductase class that catalyzes the formation of 2'-deoxyribonucleotides from the corresponding ribonucleotides using NADPH as the ultimate electron donor. The deoxyribonucleoside diphosphates are used in DNA synthesis. (From Dorland, 27th ed) EC 1.17.4.1. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Rickets: A condition caused by deficiency of vitamin D, especially in infancy and childhood, with disturbance of normal ossification. The disease is marked by bending and distortion of the bones under muscular action, by the formation of nodular enlargements on the ends and sides of the bones, by delayed closure of the fontanelles, pain in the muscles, and sweating of the head. Vitamin D and sunlight together with an adequate diet are curative, provided that the parathyroid glands are functioning properly. [EU] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Risk patient: Patient who is at risk, because of his/her behaviour or because of the type of person he/she is. [EU] Rod: A reception for vision, located in the retina. [NIH] Rosiglitazone: A drug taken to help reduce the amount of sugar in the blood. Rosiglitazone helps make insulin more effective and improves regulation of blood sugar. It belongs to the family of drugs called thiazolidinediones. [NIH] Rubber: A high-molecular-weight polymeric elastomer derived from the milk juice (latex) of Hevea brasiliensis and other trees. It is a substance that can be stretched at room temperature to atleast twice its original length and after releasing the stress, retractrapidly, and recover its original dimensions fully. Synthetic rubber is made from many different chemicals, including styrene, acrylonitrile, ethylene, propylene, and isoprene. [NIH] Rural Population: The inhabitants of rural areas or of small towns classified as rural. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Saphenous: Applied to certain structures in the leg, e. g. nerve vein. [NIH] Saphenous Vein: The vein which drains the foot and leg. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme
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dilutions. [NIH] Saralasin: 1-(N-Methylglycine)-5-L-valine-8-L-alanineangiotensin II. An octapeptide analog of angiotensin II (bovine) with amino acids 1 and 8 replaced with sarcosine and alanine, respectively. It is a highly specific competitive inhibitor of angiotensin II. [NIH] Sarcoidosis: An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands. [NIH] Sarcoplasmic Reticulum: A network of tubules and sacs in the cytoplasm of skeletal muscles that assist with muscle contraction and relaxation by releasing and storing calcium ions. [NIH] Sarcosine: Methylamino-acetic acid. [NIH] Satellite: Applied to a vein which closely accompanies an artery for some distance; in cytogenetics, a chromosomal agent separated by a secondary constriction from the main body of the chromosome. [NIH] Saturated fat: A type of fat found in greatest amounts in foods from animals, such as fatty cuts of meat, poultry with the skin, whole-milk dairy products, lard, and in some vegetable oils, including coconut, palm kernel, and palm oils. Saturated fat raises blood cholesterol more than anything else eaten. On a Step I Diet, no more than 8 to 10 percent of total calories should come from saturated fat, and in the Step II Diet, less than 7 percent of the day's total calories should come from saturated fat. [NIH] Scans: Pictures of structures inside the body. Scans often used in diagnosing, staging, and monitoring disease include liver scans, bone scans, and computed tomography (CT) or computerized axial tomography (CAT) scans and magnetic resonance imaging (MRI) scans. In liver scanning and bone scanning, radioactive substances that are injected into the bloodstream collect in these organs. A scanner that detects the radiation is used to create pictures. In CT scanning, an x-ray machine linked to a computer is used to produce detailed pictures of organs inside the body. MRI scans use a large magnet connected to a computer to create pictures of areas inside the body. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Scimitar Syndrome: Anomalous venous drainage of the right lung into the inferior vena cava, with hypoplasia of the right lung. The scimitar-shaped radiographic shadow of the anomalous vein gives the syndrome its name. [NIH] Sclera: The tough white outer coat of the eyeball, covering approximately the posterior fivesixths of its surface, and continuous anteriorly with the cornea and posteriorly with the external sheath of the optic nerve. [EU] Scleroderma: A chronic disorder marked by hardening and thickening of the skin. Scleroderma can be localized or it can affect the entire body (systemic). [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical
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structure, often a vessel or a nerve. [NIH] Sclerotherapy: Treatment of varicose veins, hemorrhoids, gastric and esophageal varices, and peptic ulcer hemorrhage by injection or infusion of chemical agents which cause localized thrombosis and eventual fibrosis and obliteration of the vessels. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Sebaceous: Gland that secretes sebum. [NIH] Sebaceous gland: Gland that secretes sebum. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Sedative: 1. Allaying activity and excitement. 2. An agent that allays excitement. [EU] Sedentary: 1. Sitting habitually; of inactive habits. 2. Pertaining to a sitting posture. [EU] Sediment: A precipitate, especially one that is formed spontaneously. [EU] Sedimentation: The act of causing the deposit of sediment, especially by the use of a centrifugal machine. [EU] Segmental: Describing or pertaining to a structure which is repeated in similar form in successive segments of an organism, or which is undergoing segmentation. [NIH] Segmentation: The process by which muscles in the intestines move food and wastes through the body. [NIH] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Seminal fluid: Fluid from the prostate and other sex glands that helps transport sperm out of the man's body during orgasm. Seminal fluid contains sugar as an energy source for sperm. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sensor: A device designed to respond to physical stimuli such as temperature, light, magnetism or movement and transmit resulting impulses for interpretation, recording, movement, or operating control. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septal: An abscess occurring at the root of the tooth on the proximal surface. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] Septicemia: Systemic disease associated with the presence and persistence of pathogenic microorganisms or their toxins in the blood. Called also blood poisoning. [EU] Septum: A dividing wall or partition; a general term for such a structure. The term is often
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used alone to refer to the septal area or to the septum pellucidum. [EU] Septum Pellucidum: A triangular double membrane separating the anterior horns of the lateral ventricles of the brain. It is situated in the median plane and bounded by the corpus callosum and the body and columns of the fornix. [NIH] Sequela: Any lesion or affection following or caused by an attack of disease. [EU] Sequence Homology: The degree of similarity between sequences. Studies of amino acid and nucleotide sequences provide useful information about the genetic relatedness of certain species. [NIH] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serologic: Analysis of a person's serum, especially specific immune or lytic serums. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH] Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Serum Albumin: A major plasma protein that serves in maintaining the plasma colloidal osmotic pressure and transporting large organic anions. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Sex Determination: The biological characteristics which distinguish human beings as female or male. [NIH] Sexually Transmitted Diseases: Diseases due to or propagated by sexual contact. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Shunt: A surgically created diversion of fluid (e.g., blood or cerebrospinal fluid) from one area of the body to another area of the body. [NIH] Sibutramine: A drug used for the management of obesity that helps reduce food intake and is indicated for weight loss and maintenance of weight loss when used in conjunction with a reduced-calorie diet. It works to suppress the appetite primarily by inhibiting the reuptake of the neurotransmitters norepinephrine and serotonin. Side effects include dry mouth, headache, constipation, insomnia, and a slight increase in average blood pressure. In some patients it causes a higher blood pressure increase. [NIH] Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU]
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Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Sleep apnea: A serious, potentially life-threatening breathing disorder characterized by repeated cessation of breathing due to either collapse of the upper airway during sleep or absence of respiratory effort. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Sneezing: Sudden, forceful, involuntary expulsion of air from the nose and mouth caused by irritation to the mucous membranes of the upper respiratory tract. [NIH] Soaps: Sodium or potassium salts of long chain fatty acids. These detergent substances are obtained by boiling natural oils or fats with caustic alkali. Sodium soaps are harder and are used as topical anti-infectives and vehicles in pills and liniments; potassium soaps are soft, used as vehicles for ointments and also as topical antimicrobials. [NIH] Social Class: A stratum of people with similar position and prestige; includes social stratification. Social class is measured by criteria such as education, occupation, and income. [NIH]
Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Social Security: Government sponsored social insurance programs. [NIH] Social Support: Support systems that provide assistance and encouragement to individuals with physical or emotional disabilities in order that they may better cope. Informal social support is usually provided by friends, relatives, or peers, while formal assistance is provided by churches, groups, etc. [NIH] Social Work: The use of community resources, individual case work, or group work to promote the adaptive capacities of individuals in relation to their social and economic environments. It includes social service agencies. [NIH]
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Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Sodium Bicarbonate: A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions. [NIH] Sodium Dodecyl Sulfate: An anionic surfactant, usually a mixture of sodium alkyl sulfates, mainly the lauryl; lowers surface tension of aqueous solutions; used as fat emulsifier, wetting agent, detergent in cosmetics, pharmaceuticals and toothpastes; also as research tool in protein biochemistry. [NIH] Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Solitary Nucleus: Gray matter located in the dorsomedial part of the medulla oblongata associated with the solitary tract. The solitary nucleus receives inputs from most organ systems including the terminations of the facial, glossopharyngeal, and vagus nerves. It is a major coordinator of autonomic nervous system regulation of cardiovascular, respiratory, gustatory, gastrointestinal, and chemoreceptive aspects of homeostasis. The solitary nucleus is also notable for the large number of neurotransmitters which are found therein. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Somatostatin: A polypeptide hormone produced in the hypothalamus, and other tissues and organs. It inhibits the release of human growth hormone, and also modulates important physiological functions of the kidney, pancreas, and gastrointestinal tract. Somatostatin receptors are widely expressed throughout the body. Somatostatin also acts as a neurotransmitter in the central and peripheral nervous systems. [NIH] Sound wave: An alteration of properties of an elastic medium, such as pressure, particle displacement, or density, that propagates through the medium, or a superposition of such alterations. [NIH] Soybean Oil: Oil from soybean or soybean plant. [NIH] Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve skeletal muscle or smooth muscle. [NIH] Spasmodic: Of the nature of a spasm. [EU] Spatial disorientation: Loss of orientation in space where person does not know which way is up. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU]
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Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrometer: An apparatus for determining spectra; measures quantities such as wavelengths and relative amplitudes of components. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Sphygmomanometer: Consisting of a blood pressure cuff which is applied to the arm and inflated to approximately 100 mm Hg, in order to distend and locate the anticubital vessel; to measure blood pressure. [NIH] Spices: The dried seeds, bark, root, stems, buds, leaves, or fruit of aromatic plants used to season food. [NIH] Spina bifida: A defect in development of the vertebral column in which there is a central deficiency of the vertebral lamina. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spinal Cord Diseases: Pathologic conditions which feature spinal cord damage or dysfunction, including disorders involving the meninges and perimeningeal spaces surrounding the spinal cord. Traumatic injuries, vascular diseases, infections, and inflammatory/autoimmune processes may affect the spinal cord. [NIH] Spinal Stenosis: Narrowing of the spinal canal. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Splenic Vein: Vein formed by the union (at the hilus of the spleen) of several small veins from the stomach, pancreas, spleen and mesentery. [NIH] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]
Stasis: A word termination indicating the maintenance of (or maintaining) a constant level; preventing increase or multiplication. [EU] Statistically significant: Describes a mathematical measure of difference between groups. The difference is said to be statistically significant if it is greater than what might be expected to happen by chance alone. [NIH] Steatosis: Fatty degeneration. [EU] Steel: A tough, malleable, iron-based alloy containing up to, but no more than, two percent carbon and often other metals. It is used in medicine and dentistry in implants and instrumentation. [NIH] Stellate: Star shaped. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become
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specialized and take the place of those that die or are lost. [NIH] Stenosis: Narrowing or stricture of a duct or canal. [EU] Stent: A device placed in a body structure (such as a blood vessel or the gastrointestinal tract) to provide support and keep the structure open. [NIH] Sterile: Unable to produce children. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]
Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stress management: A set of techniques used to help an individual cope more effectively with difficult situations in order to feel better emotionally, improve behavioral skills, and often to enhance feelings of control. Stress management may include relaxation exercises, assertiveness training, cognitive restructuring, time management, and social support. It can be delivered either on a one-to-one basis or in a group format. [NIH] Stricture: The abnormal narrowing of a body opening. Also called stenosis. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stroma: The middle, thickest layer of tissue in the cornea. [NIH] Strophanthins: A number of different cardioactive glycosides obtained from Strophanthus species. ouabain is from S. gratus and cymarine from S. kombe. They are used like the digitalis glycosides. [NIH] Stupor: Partial or nearly complete unconsciousness, manifested by the subject's responding only to vigorous stimulation. Also, in psychiatry, a disorder marked by reduced responsiveness. [EU] Styrene: A colorless, toxic liquid with a strong aromatic odor. It is used to make rubbers, polymers and copolymers, and polystyrene plastics. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subarachnoid: Situated or occurring between the arachnoid and the pia mater. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU]
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Subcutaneous: Beneath the skin. [NIH] Submandibular: Four to six lymph glands, located between the lower jaw and the submandibular salivary gland. [NIH] Submaxillary: Four to six lymph glands, located between the lower jaw and the submandibular salivary gland. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Substrate Specificity: A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts. [NIH] Suction: The removal of secretions, gas or fluid from hollow or tubular organs or cavities by means of a tube and a device that acts on negative pressure. [NIH] Sudden cardiac death: Cardiac arrest caused by an irregular heartbeat. [NIH] Sudden death: Cardiac arrest caused by an irregular heartbeat. The term "death" is somewhat misleading, because some patients survive. [NIH] Sulfates: Inorganic salts of sulfuric acid. [NIH] Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight 32.066. It is found in the amino acids cysteine and methionine. [NIH] Sulfuric acid: A strong acid that, when concentrated is extemely corrosive to the skin and mucous membranes. It is used in making fertilizers, dyes, electroplating, and industrial explosives. [NIH] Sulindac: A sulfinylindene derivative whose sulfinyl moiety is converted in vivo to an active anti-inflammatory analgesic that undergoes enterohepatic circulation to maintain constant blood levels without causing gastrointestinal side effects. [NIH] Superior Cervical Ganglion: The largest and uppermost of the paravertebral sympathetic ganglia. [NIH] Superior vena cava: Vein which returns blood from the head and neck, upper limbs, and thorax. It is formed by the union of the two brachiocephalic veins. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1. [NIH] Supine: Having the front portion of the body upwards. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Suppressive: Tending to suppress : effecting suppression; specifically : serving to suppress
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activity, function, symptoms. [EU] Suppuration: A pathologic process consisting in the formation of pus. [NIH] Suprarenal: Above a kidney. [NIH] Supraspinal: Above the spinal column or any spine. [NIH] Sural Nerve: A branch of the tibial nerve which supplies sensory innervation to parts of the lower leg and foot. [NIH] Surfactant: A fat-containing protein in the respiratory passages which reduces the surface tension of pulmonary fluids and contributes to the elastic properties of pulmonary tissue. [NIH]
Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] Sweat: The fluid excreted by the sweat glands. It consists of water containing sodium chloride, phosphate, urea, ammonia, and other waste products. [NIH] Sympathetic Nervous System: The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system. [NIH] Sympatholytics: Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the adrenergic antagonists and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals. Drugs that act in the central nervous system to reduce sympathetic activity (e.g., centrally acting alpha-2 adrenergic agonists) are included here. [NIH] Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. Called also adrenergic. [EU] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Symptomatology: 1. That branch of medicine with treats of symptoms; the systematic discussion of symptoms. 2. The combined symptoms of a disease. [EU] Synapse: The region where the processes of two neurons come into close contiguity, and the nervous impulse passes from one to the other; the fibers of the two are intermeshed, but, according to the general view, there is no direct contiguity. [NIH] Synapsis: The pairing between homologous chromosomes of maternal and paternal origin during the prophase of meiosis, leading to the formation of gametes. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptic Transmission: The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron
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releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors. These activated receptors modulate ion channels and/or secondmessenger systems to influence the postsynaptic cell. Electrical transmission is less common in the nervous system, and, as in other tissues, is mediated by gap junctions. [NIH] Synaptosomes: Pinched-off nerve endings and their contents of vesicles and cytoplasm together with the attached subsynaptic area of the membrane of the post-synaptic cell. They are largely artificial structures produced by fractionation after selective centrifugation of nervous tissue homogenates. [NIH] Syncope: A temporary suspension of consciousness due to generalized cerebral schemia, a faint or swoon. [EU] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Synostosis: The joining of contiguous and separate bones by osseous tissue. [NIH] Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systems Analysis: The analysis of an activity, procedure, method, technique, or business to determine what must be accomplished and how the necessary operations may best be accomplished. [NIH] Systole: Period of contraction of the heart, especially of the ventricles. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Systolic blood pressure: The maximum pressure in the artery produced as the heart contracts and blood begins to flow. [NIH] Systolic heart failure: Inability of the heart to contract with enough force to pump adequate amounts of blood through the body. [NIH] Systolic pressure: The highest pressure to which blood pressure rises with the contraction of the ventricles. [NIH] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Tachyphylaxis: 1. Rapid immunization against the effect of toxic doses of an extract or serum by previous injection of small doses. 2. Rapidly decreasing response to a drug or physiologically active agent after administration of a few doses. [EU] Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro. [NIH] Tamponade: The inserting of a tampon; a dressing is inserted firmly into a wound or body cavity, as the nose, uterus or vagina, principally for stopping hemorrhage. [NIH] Tardive: Marked by lateness, late; said of a disease in which the characteristic lesion is late in appearing. [EU] Tear Gases: Gases that irritate the eyes, throat, or skin. Severe lacrimation develops upon irritation of the eyes. [NIH] Telangiectasia: The permanent enlargement of blood vessels, causing redness in the skin or
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mucous membranes. [NIH] Telencephalon: Paired anteriolateral evaginations of the prosencephalon plus the lamina terminalis. The cerebral hemispheres are derived from it. Many authors consider cerebrum a synonymous term to telencephalon, though a minority include diencephalon as part of the cerebrum (Anthoney, 1994). [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Tendon: A discrete band of connective tissue mainly composed of parallel bundles of collagenous fibers by which muscles are attached, or two muscles bellies joined. [NIH] Tennis Elbow: A condition characterized by pain in or near the lateral humeral epicondyle or in the forearm extensor muscle mass as a result of unusual strain. It occurs in tennis players as well as housewives, artisans, and violinists. [NIH] Teratogenic: Tending to produce anomalies of formation, or teratism (= anomaly of formation or development : condition of a monster). [EU] Terbutaline: A selective beta-2 adrenergic agonist used as a bronchodilator and tocolytic. [NIH]
Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Tetany: 1. Hyperexcitability of nerves and muscles due to decrease in concentration of extracellular ionized calcium, which may be associated with such conditions as parathyroid hypofunction, vitamin D deficiency, and alkalosis or result from ingestion of alkaline salts; it is characterized by carpopedal spasm, muscular twitching and cramps, laryngospasm with inspiratory stridor, hyperreflexia and choreiform movements. 2. Tetanus. [EU] Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein synthesis. [NIH] Tetrahydrocannabinol: A psychoactive compound extracted from the resin of Cannabis sativa (marihuana, hashish). The isomer delta-9-tetrahydrocannabinol (THC) is considered the most active form, producing characteristic mood and perceptual changes associated with this compound. Dronabinol is a synthetic form of delta-9-THC. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] Thalassemia: A group of hereditary hemolytic anemias in which there is decreased synthesis of one or more hemoglobin polypeptide chains. There are several genetic types with clinical pictures ranging from barely detectable hematologic abnormality to severe and fatal anemia. [NIH] Thalidomide: A pharmaceutical agent originally introduced as a non-barbiturate hypnotic, but withdrawn from the market because of its known tetratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppresive and anti-angiogenic activity. It inhibits release of
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tumor necrosis factor alpha from monocytes, and modulates other cytokine action. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Thigh: A leg; in anatomy, any elongated process or part of a structure more or less comparable to a leg. [NIH] Third Ventricle: A narrow cleft inferior to the corpus callosum, within the diencephalon, between the paired thalami. Its floor is formed by the hypothalamus, its anterior wall by the lamina terminalis, and its roof by ependyma. It communicates with the fourth ventricle by the cerebral aqueduct, and with the lateral ventricles by the interventricular foramina. [NIH] Thoracic: Having to do with the chest. [NIH] Thoracic Surgery: A surgical specialty concerned with diagnosis and treatment of disorders of the heart, lungs, and esophagus. Two major types of thoracic surgery are classified as pulmonary and cardiovascular. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombocytes: Blood cells that help prevent bleeding by causing blood clots to form. Also called platelets. [NIH] Thromboembolism: Obstruction of a vessel by a blood clot that has been transported from a distant site by the blood stream. [NIH] Thrombolytic: 1. Dissolving or splitting up a thrombus. 2. A thrombolytic agent. [EU] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]
Thromboplastin: Constituent composed of protein and phospholipid that is widely distributed in many tissues. It serves as a cofactor with factor VIIa to activate factor X in the extrinsic pathway of blood coagulation. [NIH] Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thrombus: An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. Some authorities thus differentiate thrombus formation from simple coagulation or clot formation. [EU] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone,
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which helps regulate growth and metabolism. [NIH] Thyroid Gland: A highly vascular endocrine gland consisting of two lobes, one on either side of the trachea, joined by a narrow isthmus; it produces the thyroid hormones which are concerned in regulating the metabolic rate of the body. [NIH] Thyroid Hormones: Hormones secreted by the thyroid gland. [NIH] Thyrotropin: A peptide hormone secreted by the anterior pituitary. It promotes the growth of the thyroid gland and stimulates the synthesis of thyroid hormones and the release of thyroxine by the thyroid gland. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Tibial Nerve: The medial terminal branch of the sciatic nerve. The tibial nerve fibers originate in lumbar and sacral spinal segments (L4 to S2). They supply motor and sensory innervation to parts of the calf and foot. [NIH] Time Management: Planning and control of time to improve efficiency and effectiveness. [NIH]
Timolol: A beta-adrenergic antagonist similar in action to propranolol. The levo-isomer is the more active. Timolol has been proposed as an antihypertensive, antiarrhythmic, antiangina, and antiglaucoma agent. It is also used in the treatment of migraine and tremor. [NIH]
Timolol Maleate: Antihistaminic drug. [NIH] Tinnitus: Sounds that are perceived in the absence of any external noise source which may take the form of buzzing, ringing, clicking, pulsations, and other noises. Objective tinnitus refers to noises generated from within the ear or adjacent structures that can be heard by other individuals. The term subjective tinnitus is used when the sound is audible only to the affected individual. Tinnitus may occur as a manifestation of cochlear diseases; vestibulocochlear nerve diseases; intracranial hypertension; craniocerebral trauma; and other conditions. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tissue Distribution: Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios. [NIH] Tolazoline: A vasodilator that apparently has direct actions on blood vessels and also increases cardiac output. Tolazoline can interact to some degree with histamine, adrenergic, and cholinergic receptors, but the mechanisms of its therapeutic effects are not clear. It is used in treatment of persistent pulmonary hypertension of the newborn. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive
Dictionary 565
elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tonic: 1. Producing and restoring the normal tone. 2. Characterized by continuous tension. 3. A term formerly used for a class of medicinal preparations believed to have the power of restoring normal tone to tissue. [EU] Tonicity: The normal state of muscular tension. [NIH] Tonometer: For testing the intra-ocular tension. [NIH] Tonometry: The standard to determine the fluid pressure inside the eye (intraocular pressure). [NIH] Tonus: A state of slight tension usually present in muscles even when they are not undergoing active contraction. [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] Torsades de Pointes: A ventricular tachycardia characterized by periodic twisting of the points of the QRS complexes and rates between 200 and 250 beats per minute. It may be selflimited or may progress to ventricular fibrillation. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [NIH] Toxaemia: 1. The condition resulting from the spread of bacterial products (toxins) by the bloodstream. 2. A condition resulting from metabolic disturbances, e.g. toxaemia of pregnancy. [EU] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] Trabecular Meshwork: A porelike structure surrounding the entire circumference of the anterior chamber through which aqueous humor circulates to the canal of Schlemm. [NIH] Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Tracheostomy: Surgical formation of an opening into the trachea through the neck, or the opening so created. [NIH] Traction: The act of pulling. [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case
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of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfusion: The infusion of components of blood or whole blood into the bloodstream. The blood may be donated from another person, or it may have been taken from the person earlier and stored until needed. [NIH] Translating: Conversion from one language to another language. [NIH] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Trees: Woody, usually tall, perennial higher plants (Angiosperms, Gymnosperms, and some Pterophyta) having usually a main stem and numerous branches. [NIH] Tremor: Cyclical movement of a body part that can represent either a physiologic process or a manifestation of disease. Intention or action tremor, a common manifestation of cerebellar diseases, is aggravated by movement. In contrast, resting tremor is maximal when there is no attempt at voluntary movement, and occurs as a relatively frequent manifestation of Parkinson disease. [NIH] Triad: Trivalent. [NIH] Tricuspid Atresia: Absence of the orifice between the right atrium and ventricle, with the presence of an atrial defect through which all the systemic venous return reaches the left heart. As a result, there is left ventricular hypertrophy because the right ventricle is absent or not functional. [NIH] Tricuspid Valve: The valve consisting of three cusps situated between the right atrium and right ventricle of the heart. [NIH] Trigeminal: Cranial nerve V. It is sensory for the eyeball, the conjunctiva, the eyebrow, the skin of face and scalp, the teeth, the mucous membranes in the mouth and nose, and is motor to the muscles of mastication. [NIH] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Trimethaphan: A nicotinic antagonist that has been used as a ganglionic blocker in hypertension, as an adjunct to anesthesia, and to induce hypotension during surgery. [NIH] Tropoelastin: A salt-soluble precursor of elastin. Lysyl oxidase is instrumental in converting it to elastin in connective tissue. [NIH] Tropomyosin: A protein found in the thin filaments of muscle fibers. It inhibits contraction of the muscle unless its position is modified by troponin. [NIH] Troponin: One of the minor protein components of skeletal muscle. Its function is to serve as the calcium-binding component in the troponin-tropomyosin B-actin-myosin complex by
Dictionary 567
conferring calcium sensitivity to the cross-linked actin and myosin filaments. [NIH] Trypsin: A serine endopeptidase that is formed from trypsinogen in the pancreas. It is converted into its active form by enteropeptidase in the small intestine. It catalyzes hydrolysis of the carboxyl group of either arginine or lysine. EC 3.4.21.4. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberous Sclerosis: A rare congenital disease in which the essential pathology is the appearance of multiple tumors in the cerebrum and in other organs, such as the heart or kidneys. [NIH] Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] Tunica: A rather vague term to denote the lining coat of hollow organs, tubes, or cavities. [NIH]
Type 2 diabetes: Usually characterized by a gradual onset with minimal or no symptoms of metabolic disturbance and no requirement for exogenous insulin. The peak age of onset is 50 to 60 years. Obesity and possibly a genetic factor are usually present. [NIH] Tyramine: An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ubiquitin: A highly conserved 76 amino acid-protein found in all eukaryotic cells. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Ulcerative colitis: Chronic inflammation of the colon that produces ulcers in its lining. This condition is marked by abdominal pain, cramps, and loose discharges of pus, blood, and mucus from the bowel. [NIH] Ultrafiltration: The separation of particles from a suspension by passage through a filter with very fine pores. In ultrafiltration the separation is accomplished by convective transport; in dialysis separation relies instead upon differential diffusion. Ultrafiltration occurs naturally and is a laboratory procedure. Artificial ultrafiltration of the blood is referred to as hemofiltration or hemodiafiltration (if combined with hemodialysis). [NIH] Ultrasonography: The visualization of deep structures of the body by recording the reflections of echoes of pulses of ultrasonic waves directed into the tissues. Use of ultrasound for imaging or diagnostic purposes employs frequencies ranging from 1.6 to 10 megahertz. [NIH]
568 Hypertension
Ultrasound test: A test that bounces sound waves off tissues and internal organs and changes the echoes into pictures (sonograms). [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Unsaturated Fats: A type of fat. [NIH] Uraemia: 1. An excess in the blood of urea, creatinine, and other nitrogenous end products of protein and amino acids metabolism; more correctly referred to as azotemia. 2. In current usage the entire constellation of signs and symptoms of chronic renal failure, including nausea, vomiting anorexia, a metallic taste in the mouth, a uraemic odour of the breath, pruritus, uraemic frost on the skin, neuromuscular disorders, pain and twitching in the muscles, hypertension, edema, mental confusion, and acid-base and electrolyte imbalances. [EU]
Urea: A compound (CO(NH2)2), formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Ureter: One of a pair of thick-walled tubes that transports urine from the kidney pelvis to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Uric: A kidney stone that may result from a diet high in animal protein. When the body breaks down this protein, uric acid levels rise and can form stones. [NIH] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary Retention: Inability to urinate. The etiology of this disorder includes obstructive, neurogenic, pharmacologic, and psychogenic causes. [NIH] Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urinary tract infection: An illness caused by harmful bacteria growing in the urinary tract. [NIH]
Urinate: To release urine from the bladder to the outside. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Urogenital: Pertaining to the urinary and genital apparatus; genitourinary. [EU] Urogenital Diseases: Diseases of the urogenital tract. [NIH] Urokinase: A drug that dissolves blood clots or prevents them from forming. [NIH] Urologic Diseases: Diseases of the urinary tract in both male and female. It does not include the male genitalia for which urogenital diseases is used for general discussions of diseases of both the urinary tract and the genitalia. [NIH] Urology: A surgical specialty concerned with the study, diagnosis, and treatment of diseases of the urinary tract in both sexes and the genital tract in the male. It includes the specialty of andrology which addresses both male genital diseases and male infertility. [NIH] Ursodeoxycholic Acid: An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of
Dictionary 569
chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic. [NIH] Uterine Contraction: Contraction of the uterine muscle. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vacuoles: Any spaces or cavities within a cell. They may function in digestion, storage, secretion, or excretion. [NIH] Vagal: Pertaining to the vagus nerve. [EU] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vagus Nerve: The 10th cranial nerve. The vagus is a mixed nerve which contains somatic afferents (from skin in back of the ear and the external auditory meatus), visceral afferents (from the pharynx, larynx, thorax, and abdomen), parasympathetic efferents (to the thorax and abdomen), and efferents to striated muscle (of the larynx and pharynx). [NIH] Valerian: Valeriana officinale, an ancient, sedative herb of the large family Valerianaceae. The roots were formerly used to treat hysterias and other neurotic states and are presently used to treat sleep disorders. [NIH] Valine: A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway. [NIH]
Valves: Flap-like structures that control the direction of blood flow through the heart. [NIH] Vanadium: Vanadium. A metallic element with the atomic symbol V, atomic number 23, and atomic weight 50.94. It is used in the manufacture of vanadium steel. Prolonged exposure can lead to chronic intoxication caused by absorption usually via the lungs. [NIH] Varices: Stretched veins such as those that form in the esophagus from cirrhosis. [NIH] Varicose: The common ulcer in the lower third of the leg or near the ankle. [NIH] Varicose vein: An abnormal swelling and tortuosity especially of the superficial veins of the legs. [EU] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular Capacitance: Network of the finest blood vessels. [NIH] Vascular endothelial growth factor: VEGF. A substance made by cells that stimulates new blood vessel formation. [NIH] Vascular Resistance: An expression of the resistance offered by the systemic arterioles, and to a lesser extent by the capillaries, to the flow of blood. [NIH] Vasculitis: Inflammation of a blood vessel. [NIH] Vasoactive: Exerting an effect upon the calibre of blood vessels. [EU] Vasoconstriction: Narrowing of the blood vessels without anatomic change, for which constriction, pathologic is used. [NIH] Vasoconstrictor Agents: Drugs used to cause constriction of the blood vessels. [NIH] Vasodilatation: A state of increased calibre of the blood vessels. [EU] Vasodilation: Physiological dilation of the blood vessels without anatomic change. For dilation with anatomic change, dilatation, pathologic or aneurysm (or specific aneurysm) is
570 Hypertension
used. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] Vasodilator Agents: Drugs used to cause dilation of the blood vessels. [NIH] Vasomotor: 1. Affecting the calibre of a vessel, especially of a blood vessel. 2. Any element or agent that effects the calibre of a blood vessel. [EU] Vasopressins: Octapeptide antidiuretic hormones released by the neurohypophysis of all vertebrates (chemical composition varies with species). They control water metabolism and balance by regulating lung, gill, kidney, etc., and water loss, and also contract smooth muscle. They may also be neurotransmitters. Also included are synthetic vasopressin derivatives. Vasopressins are used pharmacologically as renal agents, vasoconstrictor agents, and hemostatics. [NIH] Vasopressor: 1. Stimulating contraction of the muscular tissue of the capillaries and arteries. 2. An agent that stimulates contraction of the muscular tissue of the capillaries and arteries. [EU]
VE: The total volume of gas either inspired or expired in one minute. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Vena: A vessel conducting blood from the capillary bed to the heart. [NIH] Venous: Of or pertaining to the veins. [EU] Venous blood: Blood that has given up its oxygen to the tissues and carries carbon dioxide back for gas exchange. [NIH] Venous Thrombosis: The formation or presence of a thrombus within a vein. [NIH] Ventilation: 1. In respiratory physiology, the process of exchange of air between the lungs and the ambient air. Pulmonary ventilation (usually measured in litres per minute) refers to the total exchange, whereas alveolar ventilation refers to the effective ventilation of the alveoli, in which gas exchange with the blood takes place. 2. In psychiatry, verbalization of one's emotional problems. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Ventricular Dysfunction: A condition in which the ventricles of the heart exhibit a decreased functionality. [NIH] Ventricular fibrillation: Rapid, irregular quivering of the heart's ventricles, with no effective heartbeat. [NIH] Ventricular Function: The hemodynamic and electrophysiological action of the ventricles. [NIH]
Ventricular Remodeling: The geometric and structural changes that the ventricle undergoes, usually following myocardial infarction. It comprises expansion of the infarct and dilatation of the healthy ventricle segments. While most prevalent in the left ventricle, it can also occur in the right ventricle. [NIH] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH]
Dictionary 571
Verapamil: A calcium channel blocker that is a class IV anti-arrhythmia agent. [NIH] Vertebrae: A bony unit of the segmented spinal column. [NIH] Vertebral: Of or pertaining to a vertebra. [EU] Vesicular: 1. Composed of or relating to small, saclike bodies. 2. Pertaining to or made up of vesicles on the skin. [EU] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Villous: Of a surface, covered with villi. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral Hepatitis: Hepatitis caused by a virus. Five different viruses (A, B, C, D, and E) most commonly cause this form of hepatitis. Other rare viruses may also cause hepatitis. [NIH] Viral vector: A type of virus used in cancer therapy. The virus is changed in the laboratory and cannot cause disease. Viral vectors produce tumor antigens (proteins found on a tumor cell) and can stimulate an antitumor immune response in the body. Viral vectors may also be used to carry genes that can change cancer cells back to normal cells. [NIH] Virilization: The induction or development of male secondary sec characters, especially the induction of such changes in the female, including enlargement of the clitoris, growth of facial and body hair, development of a hairline typical of the male forehead, stimulation of secretion and proliferation of the sebaceous glands (often with acne), and deepening of the voice. Called also masculinization) [EU] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Visceral Afferents: The sensory fibers innervating the viscera. [NIH] Visceral fat: One of the three compartments of abdominal fat. Retroperitoneal and subcutaneous are the other two compartments. [NIH] Visual field: The entire area that can be seen when the eye is forward, including peripheral vision. [NIH] Vitreous: Glasslike or hyaline; often used alone to designate the vitreous body of the eye (corpus vitreum). [EU] Vitreous Body: The transparent, semigelatinous substance that fills the cavity behind the crystalline lens of the eye and in front of the retina. It is contained in a thin hyoid membrane and forms about four fifths of the optic globe. [NIH] Vitreous Hemorrhage: Hemorrhage into the vitreous body. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Void: To urinate, empty the bladder. [NIH] Vomica: The profuse and sudden expectoration of pus and putrescent matter. An abnormal cavity in an organ especially in the lung, caused by suppuration and the breaking down of
572 Hypertension
tissue. [NIH] War: Hostile conflict between organized groups of people. [NIH] Weight Gain: Increase in body weight over existing weight. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]
Whooping Cough: A respiratory infection caused by Bordetella pertussis and characterized by paroxysmal coughing ending in a prolonged crowing intake of breath. [NIH] Whooping Cough: A respiratory infection caused by Bordetella pertussis and characterized by paroxysmal coughing ending in a prolonged crowing intake of breath. [NIH] Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Womb: A hollow, thick-walled, muscular organ in which the impregnated ovum is developed into a child. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xanthine: An urinary calculus. [NIH] Xanthine Oxidase: An iron-molybdenum flavoprotein containing FAD that oxidizes hypoxanthine, some other purines and pterins, and aldehydes. Deficiency of the enzyme, an autosomal recessive trait, causes xanthinuria. EC 1.1.3.22. [NIH] Xenobiotics: Chemical substances that are foreign to the biological system. They include naturally occurring compounds, drugs, environmental agents, carcinogens, insecticides, etc. [NIH]
Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]
573
INDEX 1 1-Phosphatidylinositol 3-Kinase, 445 A Abdomen, 445, 461, 468, 487, 506, 508, 513, 528, 531, 533, 534, 550, 557, 558, 563, 569 Abdominal fat, 6, 445, 571 Abdominal Pain, 421, 445, 493, 567 Aberrant, 445 Ablation, 179, 445 Abscess, 445, 553 Acatalasia, 445, 465 Acceptor, 445, 513, 530, 542 Acetic Acids, 445 Acetylcholine, 250, 256, 445, 469, 525, 526 Acidosis, 445, 450 Acne, 445, 571 Acrylonitrile, 445, 551 Actin, 445, 522, 566 Acute lymphoblastic leukemia, 445, 446 Acute lymphocytic leukemia, 445, 446 Acute renal, 446, 500 Acyl, 446 Adaptability, 446, 466, 467 Adaptation, 446, 537 Adenine, 446, 545 Adenoma, 446 Adenosine, 446, 504, 536 Adenosine Triphosphate, 446, 536 Adenosinetriphosphatase, 446 Adenovirus, 446 Adipocytes, 446, 473, 512 Adipose Tissue, 176, 445, 446, 513 Adjunctive Therapy, 446 Adjustment, 446 Adolescence, 446, 533 Adrenal Cortex, 446, 448, 475, 488, 502, 541, 549 Adrenal Glands, 335, 421, 446, 450, 548 Adrenal Medulla, 446, 465, 486, 487, 526 Adrenergic, 78, 211, 212, 231, 369, 386, 390, 404, 447, 452, 453, 456, 458, 481, 482, 487, 497, 511, 518, 519, 535, 540, 542, 545, 560, 562, 564, 567 Adrenergic Agonists, 211, 447, 560 Adrenergic Antagonists, 447, 560 Adrenergic beta-Antagonists, 447, 453 Aerobic, 229, 234, 336, 364, 371, 414, 447, 450, 489, 530
Aerobic Exercise, 234, 364, 371, 447 Aerobic Metabolism, 447, 530 Aerobic Respiration, 447, 530 Aerosol, 447 Aetiology, 447 Afferent, 447, 512, 529 Afferent Pathways, 447 Affinity, 184, 447, 448, 456, 513, 556 Afterload, 447 Agar, 447, 537 Age of Onset, 448, 567 Ageing, 448 Agonist, 448, 458, 463, 481, 518, 519, 522, 526, 535, 536, 562 Air Sacs, 422, 448, 449 Airway, 448, 461, 542, 555 Alanine, 448, 552 Albumin, 178, 448, 537 Albuminuria, 367, 448, 540 Aldehydes, 448, 572 Algorithms, 333, 448, 459 Alimentary, 448, 509, 532, 533 Alkaline, 445, 448, 449, 462, 531, 562 Alkaloid, 448, 463, 521, 526, 545 Alkalosis, 7, 448, 562 Alleles, 448, 494, 513 Allergen, 448, 478 Allograft, 448 Allopurinol, 448 Allylamine, 448, 449 Alpha Particles, 449, 546 Alpha-1, 74, 439, 449, 476, 482, 540 Alternative medicine, 245, 248, 384, 449 Aluminum, 449 Alveolar Process, 449, 549 Alveoli, 422, 449, 570 Ameliorated, 449 Ameliorating, 449 Amine, 449, 501 Amino acid, 448, 449, 451, 452, 455, 456, 480, 488, 489, 494, 496, 500, 501, 503, 512, 515, 518, 525, 528, 533, 535, 542, 543, 551, 552, 554, 559, 563, 564, 566, 567, 568, 569 Amino Acid Sequence, 449, 452, 489, 494 Amino Acid Substitution, 449, 500 Ammonia, 449, 560, 568 Ampulla, 450, 485
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Amyloid, 450, 467 Amyloidosis, 334, 450 Anaerobic, 239, 450 Anaerobic Threshold, 239, 450 Anaesthesia, 450, 506 Anal, 450, 486, 514, 529 Analgesic, 80, 450, 485, 521, 528, 545, 559 Analog, 450, 470, 492, 504, 509, 552 Analogous, 450, 482, 502, 566 Anaphylatoxins, 450, 472 Anaplasia, 450, 523 Anastomosis, 380, 450, 493, 539 Anatomical, 357, 450, 456, 460, 468, 473, 480, 484, 505, 519, 552 Anchorage, 450 Androgens, 446, 450, 475 Anemia, 239, 243, 409, 450, 458, 460, 462, 492, 521, 562 Anemia, Sickle Cell, 243, 450 Anesthesia, 448, 451, 483, 485, 541, 566 Anesthetics, 451, 457, 487 Aneurysm, 371, 451, 454, 569 Angina Pectoris, 337, 447, 449, 451, 542 Anginal, 451, 526 Angiogenesis, 451, 516 Angiogenesis Factor, 451 Angiogram, 241, 440, 451 Angiography, 241, 439, 440, 451 Angioplasty, 370, 441, 451, 522 Angiotensin-Converting Enzyme Inhibitors, 75, 186, 451, 453 Anhydrous, 451 Anionic, 452, 556 Anions, 446, 448, 452, 509, 554, 559 Ankle, 452, 569 Anode, 452 Anomalies, 452, 562 Antagonism, 255, 452, 480 Antecedent, 452 Anterior Cerebral Artery, 452, 467 Anterior chamber, 452, 509, 565 Anti-Arrhythmia Agents, 452, 480 Antiarrhythmic, 452, 564 Anti-Asthmatic Agents, 452 Antibacterial, 452, 470, 557 Antibiotic, 452, 512, 533, 557, 562 Antibodies, 452, 454, 498, 502, 505, 515, 520, 537, 546 Anticholinergic, 452, 536 Anticoagulant, 452, 543 Anticonvulsant, 452, 463, 535 Antidepressant, 257, 452
Antidiuretic, 452, 524, 570 Antiemetic, 452, 454, 469, 481, 518 Antifungal, 453, 497 Antigen, 447, 452, 453, 454, 472, 495, 501, 503, 505, 506, 507, 516, 519, 546 Antigen-Antibody Complex, 453, 472 Antihistamine, 453 Anti-infective, 453, 463, 502, 508, 555 Anti-inflammatory, 220, 453, 456, 466, 475, 479, 495, 506, 537, 559 Anti-Inflammatory Agents, 453, 456, 466, 475 Antimicrobial, 453, 478, 482 Antimycotic, 453, 470 Antineoplastic, 453, 475, 492, 503, 525 Antineoplastic Agents, 453, 525 Antioxidant, 453, 456, 493, 530, 531 Antiproliferative, 453 Antipruritic, 453, 463, 471, 476 Antipsychotic, 453, 454, 481 Antipsychotic Agents, 454, 481 Antiseptic, 454 Antiserum, 454 Antithrombotic, 454, 543 Antiviral, 454, 497, 533 Anuria, 454, 510 Anus, 450, 454, 456, 461, 472, 547 Anxiety, 235, 337, 436, 447, 454, 531, 542 Aortic Aneurysm, 454, 493 Aortic Coarctation, 454 Apnea, 454 Apnoea, 80, 454 Apolipoproteins, 454, 513 Aponeurosis, 454, 493 Apoptosis, 454 Applicability, 454 Aqueous fluid, 454, 539 Arachidonate 15-Lipoxygenase, 455, 513 Arachidonate Lipoxygenases, 455, 513 Aromatic, 455, 487, 535, 557, 558 Arrhythmia, 205, 452, 455, 571 Arteriolar, 455, 461, 490, 549 Arterioles, 455, 460, 463, 519, 522, 569 Arteriolosclerosis, 455 Arteriosclerosis, 363, 455, 467, 504 Arteriosus, 455, 544 Arteriovenous, 455, 467, 519 Arteriovenous Fistula, 455 Arteritis, 455 Articular, 455, 530 Ascorbic Acid, 455, 503, 530 Aseptic, 456, 529, 558
Index 575
Aspirin, 7, 256, 456 Assay, 456, 505, 546 Asthenia, 456 Astringents, 456, 518 Astrocytes, 456, 519, 520 Asymptomatic, 366, 445, 456, 458, 531 Ataxia, 408, 456, 562 Atenolol, 212, 456 Atopic, 456 Atresia, 456 Atrial, 337, 356, 456, 474, 523, 566 Atrial Fibrillation, 456 Atrial Natriuretic Factor, 456, 523 Atrioventricular, 456, 474 Atrium, 456, 464, 474, 545, 566, 570 Atrophy, 408, 456, 524 Attenuation, 235, 456, 521, 547 Auditory, 456, 488, 498, 516, 569 Autacoids, 457, 506 Autodigestion, 457, 531 Autoimmune disease, 176, 457, 521 Autonomic Nervous System, 250, 457, 534, 556, 560 Autonomic Neuropathy, 405, 457 Autoradiography, 457 Avian, 457 Axillary, 457, 461, 491 Axillary Artery, 457, 461 Axons, 457, 508, 529, 540, 550 Azotemia, 370, 457, 568 B Backcross, 457 Bacterial Physiology, 446, 457 Bactericidal, 457, 488 Bactericide, 457 Bacteriophage, 457, 537, 566 Bacteriuria, 457 Barbiturate, 457, 562 Baroreflex, 234, 383, 458 Basal Ganglia, 454, 456, 458, 467, 493, 521 Basal Ganglia Diseases, 456, 458, 521 Base, 334, 446, 448, 458, 478, 491, 494, 510, 562, 568 Basement Membrane, 458, 489, 511 Basilar Artery, 458, 516 Basophil, 458, 501 Benign, 75, 226, 231, 446, 455, 458, 493, 498, 523, 546 Bereavement, 375, 458 Beta blocker, 4, 6, 367, 368, 369, 371, 386, 458, 542 Beta-Thalassemia, 244, 458
Betaxolol, 213, 393, 458 Bifida, 458 Bilateral, 458 Bile, 366, 458, 459, 468, 486, 493, 502, 510, 513, 558, 568 Bile Acids, 458, 459, 558 Bile Acids and Salts, 458, 459 Bile duct, 459, 493 Bile Pigments, 459, 510 Biliary, 366, 459, 463, 531 Biliary Tract, 459, 463, 531 Bilirubin, 448, 459, 493, 503 Binding Sites, 459 Bioavailability, 79, 459 Biological therapy, 459, 497 Biomarkers, 459 Biometry, 459 Biopsy, 334, 459 Biotechnology, 73, 246, 362, 384, 403, 406, 408, 409, 459 Birth Injuries, 459 Bladder, 457, 459, 472, 492, 505, 521, 524, 543, 548, 568, 571 Blastocyst, 459, 473, 537 Blinking, 459 Blood Coagulation, 459, 460, 462, 491, 563 Blood Flow Velocity, 459 Blood Glucose, 6, 79, 370, 374, 417, 460, 500, 507 Blood Platelets, 460, 554 Blood transfusion, 460, 499 Blood Viscosity, 460, 499 Blood Volume, 460, 464 Blood-Brain Barrier, 460, 536 Blot, 460 Body Composition, 6, 460 Body Fluids, 385, 448, 459, 460, 462, 482, 556, 567 Body Image, 460 Body Mass Index, 460, 530 Body Regions, 460, 471 Bombesin, 460 Bone Density, 421, 460 Bone Marrow, 445, 446, 460, 476, 487, 494, 505, 515, 521, 522, 556 Bone scan, 460, 552 Bowel, 450, 461, 480, 492, 508, 529, 534, 558, 567 Bowel Movement, 461, 480, 558 Brachial, 250, 255, 461, 502 Brachial Artery, 250, 255, 461 Brachiocephalic Veins, 461, 559
576 Hypertension
Bradycardia, 461 Bradykinin, 250, 461, 510, 526, 537 Brain Ischemia, 461, 503 Brain Stem, 461 Breakdown, 79, 461, 480, 493, 528 Breeding, 461, 494 Bromine, 461 Bronchi, 461, 462, 487, 509, 565 Bronchial, 461, 501, 543 Bronchiectasis, 413, 461 Bronchioles, 449, 461, 544 Bronchiolitis, 461 Bronchiseptica, 461, 535 Bronchitis, 461, 469 Bronchodilator, 461, 509, 562 Bronchopulmonary, 7, 413, 461 Bronchopulmonary Dysplasia, 7, 413, 461 Bronchoscopy, 387, 412, 462 Buccal, 462, 515 Buffers, 458, 462 Bumetanide, 462 Bypass, 370, 462, 522 C Cadmium, 369, 462 Cadmium Poisoning, 462 Calcification, 455, 462 Calcineurin, 462 Calcium, 81, 176, 177, 179, 180, 181, 182, 186, 227, 253, 254, 257, 337, 341, 355, 359, 367, 368, 369, 371, 372, 385, 386, 387, 390, 417, 418, 442, 449, 452, 453, 462, 463, 469, 470, 472, 480, 490, 516, 519, 522, 525, 526, 530, 532, 544, 552, 555, 562, 566, 571 Calcium Channels, 462, 519 Calcium Oxalate, 463, 530 Calculi, 463, 497 Callus, 463, 484 Calmodulin, 462, 463 Calsequestrin, 463 Camphor, 463 Cannabidiol, 463 Cannabinoids, 463 Cannabinol, 463 Capillary, 205, 421, 422, 461, 463, 495, 513, 539, 544, 570 Capillary Permeability, 461, 463 Capsaicin, 463 Capsules, 463, 494, 495 Captopril, 178, 214, 241, 370, 463 Carbachol, 391, 463 Carbamazepine, 463
Carbohydrate, 463, 475, 496, 527 Carbon Dioxide, 239, 463, 464, 465, 477, 493, 537, 549, 570 Carbonate Dehydratase, 464 Carbonic Anhydrase Inhibitors, 464 Carboxy, 464 Carcinogenic, 464, 468, 471, 506, 528, 542, 558 Carcinogens, 464, 471, 522, 528, 530, 572 Cardenolides, 464 Cardiac Glycosides, 464, 480 Cardiogenic, 464 Cardiomyopathy, 205, 464 Cardiopulmonary, 464, 499, 521 Cardiopulmonary Bypass, 464, 499 Cardiorespiratory, 447, 464 Cardioselective, 456, 458, 464, 542 Cardiotonic, 464, 480, 481, 535 Cardiovascular Agents, 464 Cardiovascular Physiology, 465 Cardiovascular System, 227, 374, 457, 465 Carnitine, 181, 186, 465 Carotene, 212, 465, 550 Carotid Arteries, 465 Carotid Body, 465, 468 Carotid Sinus, 465, 540 Carrier Proteins, 465, 537, 546 Case report, 74, 465, 470 Case series, 465, 470 Catabolism, 465 Catalase, 445, 465 Catecholamine, 228, 465, 481, 535 Catheter, 239, 249, 465, 485, 499, 508 Catheterization, 240, 451, 465, 508, 522 Cathode, 452, 466 Cations, 466, 509 Caudal, 466, 479, 504, 539 Causal, 466, 486 Causality, 466 Cause of Death, 365, 423, 466 Caveolae, 466 Caveolins, 466 Celecoxib, 466 Celiac Artery, 466, 500 Cell Adhesion, 466, 507 Cell Adhesion Molecules, 466 Cell Death, 454, 466, 495 Cell Differentiation, 466, 555 Cell Division, 408, 457, 466, 477, 497, 517, 520, 537, 542, 553 Cell membrane, 462, 465, 466, 471, 478, 489, 493, 509, 510, 536, 539
Index 577
Cell Membrane Structures, 466 Cell proliferation, 455, 466, 555 Cell Respiration, 447, 466, 530, 549 Cell Size, 467, 491 Cell Survival, 467, 497 Cellulose, 467, 537 Central Nervous System Infections, 467, 498 Centrifugation, 467, 519, 561 Ceramide, 467 Cerebellar, 456, 467, 547, 566 Cerebral Angiography, 467, 515 Cerebral Arteries, 458, 467 Cerebral Cortex, 456, 467, 488 Cerebral hemispheres, 458, 461, 467, 468, 562 Cerebral Hemorrhage, 467 Cerebral Infarction, 467 Cerebral Palsy, 375, 467 Cerebral Veins, 467 Cerebrospinal, 423, 468, 469, 554 Cerebrospinal fluid, 423, 468, 469, 554 Cerebrospinal Fluid Pressure, 423, 468 Cerebrum, 467, 468, 562, 567 Cervical, 468, 536 Cervix, 468, 491 Character, 451, 468, 478 Chemoreceptor, 454, 468 Chemotactic Factors, 468, 472 Chemotherapeutic agent, 468, 480 Chenodeoxycholic Acid, 468, 568 Chest Pain, 387, 412, 468 Chest wall, 468, 538 Chin, 468, 517 Chiropractic, 208, 468 Chlorine, 468 Chlorogenic Acid, 468 Choleretic, 468, 469, 569 Cholesterol Esters, 469, 513 Cholinergic, 82, 178, 453, 463, 469, 526, 564 Choroid, 469, 474, 550 Choroid Plexus, 469 Chromaffin System, 469, 485 Chromatin, 454, 469, 486 Chromosomal, 82, 469, 537, 552 Chronic Disease, 176, 338, 416, 469, 471 Chronic Obstructive Pulmonary Disease, 184, 469 Chronic renal, 182, 334, 366, 378, 469, 493, 538, 568 Chylomicrons, 469, 513 Chymopapain, 469, 531
Ciliary, 414, 454, 455, 469, 527 Ciliary Arteries, 455, 469 Ciliary Body, 455, 469 Ciliary processes, 454, 455, 469 Cinnarizine, 469 Circadian, 179, 469, 470 Circadian Rhythm, 470 Circulatory system, 470, 485, 508 CIS, 470, 550 Citric Acid, 470 Citrus, 455, 470 Clamp, 470 Clear cell carcinoma, 470, 478 Cleave, 470 Climacteric, 470 Clindamycin, 470 Clinical Medicine, 183, 192, 344, 470, 540 Clinical Protocols, 470 Clinical study, 178, 470, 474 Cloning, 358, 459, 470, 512 Cloprostenol, 470 Clot Retraction, 470, 537 Clotrimazole, 470 Coagulation, 192, 459, 471, 500, 537, 563 Coal, 471, 523 Coal Tar, 471, 523 Coenzyme, 214, 455, 471 Cofactor, 471, 543, 563 Cognition, 471 Cognitive restructuring, 471, 558 Cohort Studies, 471, 486 Colic, 471 Colitis, 471 Collagen, 449, 458, 471, 473, 489, 491, 494, 502, 516, 538, 542 Collagen disease, 471, 502 Collapse, 461, 471, 538, 555 Colloidal, 448, 471, 484, 554 Colon, 408, 471, 472, 511, 567 Colorectal, 472 Combination Therapy, 338, 361, 368, 472, 488 Comorbidity, 4, 472 Complement, 450, 472, 494, 507, 516, 537 Complementary and alternative medicine, 191, 224, 472 Complementary medicine, 472 Complete remission, 472, 548 Compress, 472, 500 Computational Biology, 403, 406, 473 Computed tomography, 239, 387, 460, 473, 552
578 Hypertension
Computerized tomography, 473 Concentric, 455, 473 Conception, 473, 490, 558 Concomitant, 404, 473 Conduction, 452, 473 Cones, 473, 550 Confounding, 473 Conjugated, 459, 468, 473, 477 Conjunctiva, 469, 473, 520, 536, 566 Connective Tissue Cells, 473 Connective Tissue Diseases, 473 Consciousness, 436, 437, 450, 473, 478, 481, 544, 549, 561 Constipation, 385, 454, 473, 492, 554 Constrict, 249, 387, 473, 522 Constriction, 249, 473, 509, 520, 527, 544, 552, 569 Constriction, Pathologic, 473, 569 Consumption, 176, 239, 254, 369, 473, 479, 493, 531 Contamination, 192, 473 Continuous infusion, 254, 474 Contractility, 235, 236, 451, 474 Contraindications, ii, 9, 474 Contralateral, 474, 528, 547 Contrast Media, 474, 515 Contrast medium, 451, 467, 474 Controlled clinical trial, 367, 474, 547 Controlled study, 474 Conus, 474, 544 Convulsions, 452, 457, 474, 483, 504, 540 Coordination, 437, 474, 521 Cor, 474 Cor pulmonale, 474 Cornea, 452, 454, 455, 474, 520, 552, 558 Coronary Arteriosclerosis, 474, 522 Coronary Artery Bypass, 474 Coronary Circulation, 451, 475, 526 Coronary Disease, 245, 253, 475 Coronary Thrombosis, 475, 518, 522 Coronary Vasospasm, 475 Coronary Vessels, 475 Corpus, 475, 533, 541, 554, 563, 571 Corpus Luteum, 475, 541 Cortex, 209, 421, 475, 488, 547 Cortical, 475, 488, 553, 562 Corticosteroid, 421, 475 Cortisol, 448, 475 Cortisone, 475, 479 Cost Savings, 475 Cost-benefit, 475 Cost-Benefit Analysis, 475
Cranial, 468, 476, 498, 508, 524, 527, 529, 534, 566, 569 Craniocerebral Trauma, 458, 467, 476, 498, 562, 564 Craniotomy, 476 Creatinine, 365, 385, 440, 476, 510, 568 Creatinine clearance, 476 Criterion, 476 Crossing-over, 476, 547 Cross-Sectional Studies, 476, 486 Crystalluria, 476 Cultured cells, 476 Curative, 476, 551, 563 Cutaneous, 476, 509, 515 Cyanosis, 422, 476, 500 Cyclic, 463, 476, 497, 526, 536, 539, 542 Cyclin, 476 Cyclodextrins, 476 Cyclooxygenase Inhibitors, 476 Cyclosporine, 76, 215, 476 Cyproheptadine, 476 Cyst, 476 Cystathionine beta-Synthase, 476, 503 Cytochrome, 477 Cytogenetics, 477, 552 Cytokine, 477, 563 Cytoplasm, 454, 466, 477, 486, 497, 551, 552, 561 Cytoskeleton, 477, 507 Cytotoxic, 463, 477, 546, 555 Cytotoxicity, 83, 448, 477 D Dairy Products, 182, 477, 511, 552 Day Care, 386, 477 Deamination, 477, 520, 568 Decarboxylation, 477, 501, 518 Decidua, 477, 537 Decision Making, 477 Decompensation, 449, 477 Decompression, 380, 477, 514 Decongestant, 478, 535 Defense Mechanisms, 478, 507 Degenerative, 228, 474, 478, 500, 515, 529, 550 Dehydration, 421, 478 Deja Vu, 478 Deletion, 454, 478, 494 Delivery of Health Care, 478, 498 Dementia, 8, 385, 453, 454, 478 Dendrites, 478, 525 Dendritic, 478, 517, 550
Index 579
Density, 77, 372, 460, 467, 478, 483, 491, 513, 528, 547, 556 Dental Caries, 176, 478, 491 Depolarization, 478, 555 Depressive Disorder, 478, 513 Deprivation, 478 Dermatitis, 478 DES, 182, 184, 450, 478 Desensitization, 235, 478 Detergents, 478, 491 Detoxification, 479 Deuterium, 479, 502 Deuterium Oxide, 479 Developed Countries, 479 Dexamethasone, 479 Dextrorotatory, 479 Diabetes Insipidus, 479, 502 Diabetic Retinopathy, 373, 405, 426, 479, 536 Diagnostic procedure, 261, 384, 479 Dialysate, 479 Dialyzer, 479, 499 Diarrhea, 385, 479, 492 Diastole, 479 Diastolic pressure, 479, 503 Dichloroacetate, 479 Diencephalon, 479, 504, 562, 563 Dietary Fats, 369, 479, 513 Digestion, 448, 458, 459, 461, 480, 508, 513, 533, 558, 569 Digestive system, 259, 480 Digestive tract, 5, 457, 480, 555 Digitalis, 464, 480, 530, 558 Digitalis Glycosides, 480, 558 Dihydropyridines, 480 Dihydrotestosterone, 480, 547 Dilatation, 451, 461, 480, 501, 508, 541, 569, 570 Dilatation, Pathologic, 480, 569 Dilate, 249, 480 Dilated cardiomyopathy, 76, 480 Dilation, 461, 480, 522, 569, 570 Dilator, 480, 526 Diltiazem, 215, 387, 480 Dimethyl, 480, 525, 526 Dipeptides, 480 Diploid, 480, 537 Dipyridamole, 480 Discrete, 251, 480, 514, 562 Disease Progression, 480 Disinfectant, 480, 488 Disparity, 480
Dissection, 76, 480 Dissociation, 447, 481 Dissociative Disorders, 481 Distal, 380, 475, 481, 510, 540, 544 Diuresis, 340, 481 Diuretics, Thiazide, 391, 453, 481 Dizziness, 387, 437, 481 Dobutamine, 74, 481 Docosahexaenoic Acids, 481 Domesticated, 481, 497 Domperidone, 481 Dopamine, 453, 481, 518, 520, 525, 535 Dopamine Antagonists, 481 Dorsal, 481, 539 Dosage schedule, 481 Dose-dependent, 482 Double-blind, 247, 248, 366, 482 Doxazosin, 83, 216, 392, 482 Doxycycline, 482 Drip, 482 Drive, ii, vi, 9, 175, 369, 373, 482, 509, 512 Drug Design, 396, 426, 482 Drug Interactions, 395, 482 Drug Tolerance, 482, 564 Drug Toxicity, 482 Drusen, 482 Dry Eye Syndrome, 426, 482 Duct, 450, 465, 482, 489, 532, 551, 558 Ductus Arteriosus, 482 Dumping Syndrome, 476, 482 Duodenum, 458, 482, 485, 500, 510, 525, 558 Dyes, 450, 482, 491, 526, 559 Dyskinesia, 414, 454, 482 Dyslipidemia, 231, 372, 374, 483 Dysmenorrhea, 483, 537 Dyspareunia, 483, 488 Dysphoric, 478, 483 Dysplasia, 409, 421, 422, 483, 521 Dystrophy, 408, 483 E Echocardiography, 483 Eclampsia, 253, 483, 540 Ectopic, 180, 483 Effector, 445, 472, 483, 524, 536 Effector cell, 483, 524 Efferent, 483 Effusion, 483 Eicosanoids, 476, 483 Ejaculation, 483, 553 Elastic, 483, 556, 560 Elasticity, 455, 474, 483
580 Hypertension
Elastin, 229, 471, 473, 483, 489, 566 Electroacupuncture, 248, 483 Electrocardiogram, 239, 483 Electrocoagulation, 471, 483 Electrolysis, 452, 466, 483, 484 Electrolyte, 448, 475, 484, 499, 510, 519, 539, 544, 556, 568 Electrophoresis, 484 Electrophysiological, 484, 570 Electroplating, 484, 559 Emboli, 484 Embolization, 484 Embolus, 484, 506 Embryo, 459, 466, 484, 506 Embryogenesis, 484 Emergency Treatment, 5, 484 Emesis, 454, 484, 503 Emollient, 484, 496 Emphysema, 469, 484 Empirical, 484 Emulsion, 457, 484 Enalapril, 8, 216, 392, 484 Enamel, 478, 484 Encapsulated, 484 Encephalopathy, 484 Endarterectomy, 451, 485 Endemic, 485, 557 Endocardium, 485 Endocrine Glands, 485, 532 Endocrine System, 485, 524 Endocrinology, 180, 340, 341, 485 Endocytosis, 466, 485 Endogenous, 77, 357, 447, 460, 481, 483, 485, 486, 488, 528, 530, 543, 565 Endometrial, 485 Endometrium, 477, 485, 517 Endorphin, 248, 485 Endoscope, 485 Endoscopic, 4, 8, 365, 369, 462, 485 Endoscopy, 5, 365, 485 Endothelium, Lymphatic, 485 Endothelium, Vascular, 485 Endothelium-derived, 485, 526 Endotoxic, 485, 513 Endotoxins, 472, 485, 486, 510 End-stage renal, 469, 486, 538 Energy balance, 486, 512 Energy Intake, 486 Enhancers, 177, 486 Enkephalins, 486, 525, 528 Enterohepatic, 486, 559 Enterohepatic Circulation, 486, 559
Enteropeptidase, 486, 567 Environmental Exposure, 486, 528 Environmental Health, 402, 404, 486 Enzyme Inhibitors, 81, 371, 372, 486, 537 Eosinophils, 486, 497, 512 Epidemic, 374, 486, 557 Epidemiologic Studies, 486 Epidemiological, 228, 253, 486 Epidermal, 486, 517 Epidermal Growth Factor, 486 Epidermis, 486, 487, 545 Epigastric, 487, 531 Epinephrine, 357, 447, 481, 487, 509, 525, 526, 567 Epithelial, 74, 446, 469, 477, 487, 500, 511, 519 Epithelial Cells, 487, 500, 511, 519 Epithelium, 458, 485, 487, 509 Epitope, 487 Epoprostenol, 253, 254, 392, 396, 487, 504 Epoxide Hydrolases, 487 Erectile, 206, 487, 533 Erection, 487, 536, 541 Ergometer, 487 Ergometry, 341, 487 Erythrocyte Volume, 460, 487 Erythrocytes, 450, 460, 464, 487, 547 Erythropoietin, 364, 487 Esophageal, 3, 5, 6, 244, 366, 369, 380, 487, 553 Esophageal and Gastric Varices, 244, 366, 487 Esophageal Varices, 3, 5, 6, 369, 380, 487, 553 Esophagus, 456, 480, 487, 488, 535, 548, 558, 563, 569 Essential Tremor, 408, 488 Estradiol, 488 Estrogen, 488, 541 Estrogen receptor, 488 Estrogen Replacement Therapy, 488 Ethanol, 226, 488 Ethanolamine, 488, 519 Ether, 488 Ethnic Groups, 488 Eukaryotic Cells, 488, 505, 529, 567 Evacuation, 473, 488 Evoke, 488, 558 Evoked Potentials, 488 Excipient, 488 Excitability, 452, 488, 523, 545 Excitation, 468, 488, 491, 525
Index 581
Excitatory, 488, 496 Excitatory Amino Acids, 488 Excrete, 454, 489, 510, 548 Exercise Test, 489 Exercise Tolerance, 240, 489 Exhaustion, 452, 489 Exocrine, 489, 531 Exocytosis, 489, 501 Exogenous, 463, 481, 485, 489, 543, 567 Exon, 489 Extensor, 489, 562 Extracellular Matrix, 473, 489, 491, 507, 516 Extracellular Matrix Proteins, 489, 516 Extracellular Space, 489, 519 Extracorporeal, 489, 499 Extraction, 489 Extraocular, 489 Extrapyramidal, 453, 481, 489 Extrarenal, 489 Extravasation, 489, 499 Eye Infections, 446, 490 F Facial, 490, 516, 532, 556, 571 Family Planning, 403, 490 Family Practice, 490 Fasciculation, 490, 524 Fatigue, 385, 421, 437, 490, 499 Fatty acids, 176, 448, 481, 483, 490, 496, 513, 542, 555 Fatty Liver, 490 Fatty Liver, Alcoholic, 490 Feces, 473, 490, 558 Felodipine, 216, 392, 490 Femoral, 240, 464, 490 Femoral Artery, 464, 490 Femur, 490 Fenfluramine, 490 Fertilizers, 490, 526, 559 Fetal Blood, 482, 490 Fetal Death, 490 Fetus, 487, 490, 537, 540, 569 Fibrillation, 490 Fibrin, 459, 470, 490, 491, 537, 563 Fibrinogen, 77, 372, 490, 537, 563 Fibrinolysis, 363, 491 Fibroblasts, 473, 491, 507 Fibromuscular Dysplasia, 370, 491 Fibronectins, 489, 491 Fibrosis, 350, 409, 449, 491, 552, 553 Filtration, 385, 491, 510 Fish Oils, 367, 481, 491
Fistula, 491 Flatus, 491, 493 Flexion, 491 Flow Cytometry, 491 Fluorescence, 236, 491 Fluorescent Dyes, 491 Fluorine, 491 Fluorouracil, 480, 492 Flushing, 492 Flutter, 492 Folate, 492 Fold, 492, 518, 528, 531 Folic Acid, 176, 492 Follicles, 492 Folliculitis, 492 Foramen, 468, 492, 516, 534 Forearm, 249, 255, 256, 460, 492, 562 Fosinopril, 370, 492 Fossa, 492 Fourth Ventricle, 469, 492, 563 Fractionation, 492, 561 Free Radicals, 453, 481, 492, 522 Frontal Lobe, 452, 467, 492 Fructose, 492, 496, 508 Functional Disorders, 492 Fundus, 491, 492, 529 Furosemide, 492, 506 G Gait, 493 Gallate, 493 Gallbladder, 365, 445, 459, 480, 492, 493, 500 Gallstones, 459, 468, 493, 569 Gamma Rays, 493, 546 Ganglia, 445, 458, 493, 524, 534, 559, 560 Ganglion, 228, 493, 527, 529, 550 Ganglionic Blockers, 453, 493 Gap Junctions, 493, 561 Gas exchange, 450, 493, 544, 549, 570 Gastrectomy, 476, 493 Gastric, 365, 457, 460, 465, 466, 486, 487, 493, 501, 502, 533, 553 Gastric Bypass, 493 Gastric Fundus, 487, 493 Gastrin, 493, 501 Gastroenteritis, 461, 493 Gastrointestinal tract, 366, 488, 494, 512, 554, 556, 558, 567 Gavage, 494 Gelatin, 494, 496, 563 Gels, 494 Gene Deletion, 494
582 Hypertension
Gene Expression, 182, 230, 409, 494 Gene Expression Profiling, 494 Gene Frequency, 494 Gene Therapy, 81, 373, 446, 494 General practitioner, 364, 494 Genetic Code, 494, 527 Genetic Engineering, 459, 470, 494 Genetic Markers, 494 Genetic Predisposition to Disease, 494 Genetics, 75, 176, 245, 255, 353, 477, 494, 520 Genital, 457, 470, 495, 508, 568 Genomics, 182, 495 Genotype, 75, 176, 495, 535 Germ Cells, 495, 517, 528, 530, 556, 562 Germline mutation, 495, 501 Gestation, 228, 495, 534, 537, 540 Gestational, 206, 495 Giant Cells, 495, 552 Ginseng, 211, 212, 217, 221, 222, 495 Glomerular, 334, 364, 495, 508, 510, 526, 548 Glomerular Filtration Rate, 495, 510, 526 Glomeruli, 495, 545 Glomerulonephritis, 334, 495 Glomerulosclerosis, 334, 495 Glomerulus, 495, 523 Glottis, 495, 501, 535 Glucans, 476, 495 Glucocorticoid, 77, 233, 355, 479, 495, 502, 519 Glucose Intolerance, 360, 479, 496 Glucose tolerance, 496 Glucose Tolerance Test, 496 Glucuronic Acid, 496, 500 Glutamate, 83, 496 Glutamic Acid, 492, 496, 500, 525, 542 Glutathione Peroxidase, 496 Glycerol, 496, 536 Glycerophospholipids, 496, 536 Glycine, 449, 459, 468, 496, 525, 554 Glycolysis, 496 Glycoprotein, 487, 490, 495, 496, 497, 511, 563, 567 Glycosaminoglycans, 212, 489, 496 Glycoside, 496, 502, 530, 551 Gonadal, 496, 558 Gout, 206, 417, 496 Governing Board, 497, 540 Gp120, 497, 533 Grade, 497 Graft, 497, 502, 505, 522
Grafting, 474, 497, 505 Gram-negative, 461, 485, 497, 550 Gram-positive, 497, 511 Granulocytes, 458, 497, 512, 555, 572 Grasses, 492, 497 Growth factors, 497, 519 Growth Plate, 180, 497 Guanethidine, 392, 497 Guanidines, 497 Guanylate Cyclase, 497, 526 Guideline Adherence, 497 Guinea Pigs, 497 H Habitat, 498 Haemodialysis, 498 Hair Cells, 498, 516 Hair follicles, 492, 498 Half-Life, 498, 504, 537 Hantavirus, 413, 498 Haploid, 498, 537 Haplotypes, 498 Haptens, 447, 498, 546 Headache, 437, 498, 503, 504, 554 Headache Disorders, 498 Health Behavior, 233, 234, 498 Health Care Costs, 498, 499 Health Education, 226, 234, 235, 257, 358, 379, 412, 415, 424, 498 Health Expenditures, 498, 499 Health Promotion, 191, 375, 416, 499 Health Services, 251, 478, 499 Health Status, 498, 499 Heart Atrium, 499 Heart attack, 371, 378, 465, 499 Heart Catheterization, 239, 387, 499 Heartbeat, 437, 499, 559, 570 Heart-Lung Transplantation, 499 Hematology, 499 Hematoma, 499, 500 Hematuria, 334, 499 Heme, 459, 477, 499, 500, 531, 538, 539 Hemodiafiltration, 499, 567 Hemodialysis, 364, 479, 499, 510, 567 Hemodilution, 499 Hemodynamics, 352, 499, 510 Hemofiltration, 499, 567 Hemoglobin, 6, 79, 239, 450, 451, 458, 476, 487, 499, 500, 512, 531, 539, 562 Hemoglobin E, 240, 500 Hemoglobin M, 240, 476, 500 Hemoglobinopathies, 494, 500 Hemoglobinuria, 408, 500
Index 583
Hemolytic, 450, 500, 562 Hemorrhagic stroke, 177, 500 Hemorrhoids, 500, 553 Hemostasis, 182, 500, 507, 554 Heparin, 500 Hepatic Artery, 500 Hepatic Veins, 9, 500 Hepatitis, 206, 239, 244, 490, 500, 571 Hepatocytes, 500 Hepatopulmonary Syndrome, 500 Hereditary, 473, 495, 496, 501, 544, 550, 562 Hereditary mutation, 495, 501 Heredity, 417, 494, 495, 501 Hernia, 501 Heterodimers, 501, 507 Heterogeneity, 78, 342, 447, 501 Hiccup, 481, 501 High-Frequency Jet Ventilation, 501 High-Frequency Ventilation, 79, 501 Histamine, 450, 453, 469, 476, 501, 564 Histamine Release, 450, 501 Histidine, 501 Histology, 501 Homeostasis, 357, 501, 556 Homicide, 375, 501 Homogeneous, 455, 501 Homologous, 448, 476, 494, 499, 501, 553, 560 Hormonal, 249, 421, 456, 475, 488, 501 Hormone Replacement Therapy, 502 Host, 457, 502, 505, 512, 571 Humeral, 502, 562 Humoral, 502 Humour, 502 Hybrid, 457, 502 Hybridization, 502, 520 Hybridomas, 502, 507 Hydralazine, 218, 392, 394, 502 Hydration, 464, 502 Hydrochloric Acid, 502 Hydrochlorothiazide, 8, 179, 340, 390, 391, 392, 393, 394, 502 Hydrocortisone, 421, 502 Hydrogen Peroxide, 465, 496, 502, 513, 559 Hydrolases, 502, 536 Hydrolysis, 446, 503, 509, 533, 536, 544, 567 Hydrophobic, 479, 496, 503, 513 Hydroxyeicosatetraenoic Acids, 455, 503 Hydroxylysine, 471, 503
Hydroxyproline, 449, 471, 503 Hydroxyurea, 503 Hygienic, 248, 503 Hyperaldosteronism, 250, 503 Hyperbilirubinemia, 503, 510 Hypercholesterolemia, 207, 256, 483, 503 Hyperglycemia, 373, 374, 503 Hyperhomocysteinemia, 477, 503 Hyperlipidaemia, 503 Hyperlipidemia, 355, 373, 483, 503 Hyperoxaluria, 503 Hyperplasia, 80, 503 Hypersensitivity, 448, 478, 503, 512, 550 Hypertension, Renal, 365, 503 Hypertension, Renovascular, 503 Hypertensive Encephalopathy, 503 Hyperthyroidism, 504, 542 Hypertriglyceridemia, 483, 504 Hypertrophic cardiomyopathy, 504 Hyperuricemia, 372, 497, 504 Hypnotic, 457, 504, 562 Hypoglycaemia, 504 Hypoglycemia, 504 Hypoplasia, 504, 552 Hypotension, 235, 374, 405, 421, 454, 474, 493, 504, 519, 525, 566 Hypothalamic, 178, 504 Hypothalamus, 457, 479, 504, 523, 525, 537, 556, 563 Hypothermia, 499, 504 Hypoventilation, 504 Hypoxanthine, 504, 572 Hypoxemia, 504 Hypoxic, 227, 451, 504 I Id, 185, 204, 413, 418, 419, 420, 432, 434, 504 Idiopathic, 350, 407, 491, 504, 552 Ileum, 504, 510, 525 Iloprost, 504 Imidazole, 470, 501, 504 Immersion, 504, 523 Immune response, 176, 453, 457, 475, 498, 504, 505, 516, 559, 571 Immune system, 459, 483, 504, 505, 512, 515, 521, 535, 569, 572 Immunity, 448, 505, 515, 528 Immunization, 505, 541, 561 Immunoassay, 505 Immunodeficiency, 408, 417, 505 Immunodeficiency syndrome, 417, 505 Immunogenic, 505, 513, 546
584 Hypertension
Immunoglobulin, 452, 505, 520 Immunohistochemistry, 505 Immunologic, 468, 505, 515, 546 Immunology, 426, 447, 491, 505 Immunophilin, 462, 505 Immunosuppressant, 492, 505 Immunosuppressive, 462, 495, 505, 561 Immunotherapy, 459, 478, 505 Implantation, 473, 505 Impotence, 375, 487, 505 In situ, 505 In Situ Hybridization, 505 In vivo, 494, 500, 505, 519, 530, 559, 561, 563 Incision, 505, 508 Incontinence, 375, 385, 505, 529 Incubation, 506, 511, 535 Incubation period, 506, 511, 535 Indapamide, 218, 382, 392, 506 Indicative, 335, 506, 532, 569 Indomethacin, 506 Indoramin, 506 Induction, 74, 450, 453, 493, 506, 541, 571 Infancy, 506, 544, 551 Infant Mortality, 375, 424, 506 Infarction, 4, 79, 207, 245, 371, 454, 461, 467, 475, 481, 500, 506, 518, 522, 538, 542, 549, 570 Inferior vena cava, 506, 552 Infertility, 375, 506, 568 Infiltration, 495, 506, 541 Infusion, 239, 254, 255, 506, 522, 553, 566 Ingestion, 462, 496, 506, 518, 521, 538, 562 Inhalation, 350, 447, 501, 506, 538 Initiation, 74, 506, 565 Innervation, 507, 520, 560, 564 Inorganic, 507, 521, 535, 559 Inotropic, 456, 481, 490, 507 Inpatients, 507 Insecticides, 507, 572 Insight, 425, 507 Insomnia, 507, 554 Instillation, 507 Insulator, 507, 521 Insulin-dependent diabetes mellitus, 507 Insulin-like, 507 Integrins, 507 Intensive Care, 5, 239, 507 Intensive Care Units, 507 Interindividual, 255, 507 Interleukin-6, 507 Intermittent, 482, 507, 514, 534
Interneurons, 507 Interstitial, 232, 489, 508, 523, 548 Intestinal, 83, 245, 465, 468, 486, 496, 508, 516 Intestine, 459, 461, 486, 508, 511, 534 Intoxication, 508, 569, 572 Intracellular Membranes, 508, 517 Intracranial Aneurysm, 467, 508 Intracranial Pressure, 468, 508, 544 Intrahepatic, 4, 9, 365, 369, 508 Intramuscular, 508, 532 Intramuscular injection, 508 Intraocular, 179, 237, 242, 246, 508, 527, 565 Intravascular, 499, 508 Intravenous, 239, 506, 508, 532 Intrinsic, 447, 458, 501, 508 Intubation, 465, 508 Inulin, 495, 508 Invasive, 505, 508, 515, 531 Involuntary, 458, 459, 488, 490, 508, 522, 536, 547, 555, 556 Involution, 508 Iodine, 508 Ion Channels, 456, 509, 535, 561 Ion Pumps, 509 Ion Transport, 255, 509, 519 Ionizing, 449, 486, 509, 546 Ions, 235, 364, 458, 462, 463, 464, 481, 484, 502, 509, 539, 544, 552 Iris, 452, 455, 469, 474, 509, 539, 545 Irritants, 509 Ischemia, 364, 456, 461, 500, 509, 522, 549 Ischemic stroke, 509 Islet, 509 Isometric Contraction, 509 Isopropyl, 178, 509 Isoproterenol, 509 Isosorbide, 509 Isosorbide Dinitrate, 509 Isotonic, 510 J Jaundice, 366, 503, 510 Jejunum, 493, 510 Joint, 78, 362, 367, 404, 455, 510, 529, 560, 561 K Kallidin, 461, 510 Kallikrein-Kinin System, 510 Kb, 402, 510 Keratolytic, 478, 510 Keto, 510
Index 585
Kidney Cortex, 510 Kidney Failure, 334, 385, 486, 495, 510 Kidney Failure, Acute, 510 Kidney Failure, Chronic, 385, 510 Kidney Glomerulus, 510 Kidney stone, 385, 511, 530, 548, 568 Kidney Transplantation, 416, 510, 511 Kinetics, 462, 511 L Labetalol, 219, 350, 511 Labile, 472, 511 Lactation, 511, 531, 541 Lactococcus, 178, 511 Lactococcus lactis, 178, 511 Laminin, 458, 489, 511 Large Intestine, 480, 508, 511, 547, 555 Larynx, 495, 511, 565, 569 Latency, 511 Latent, 494, 511, 540 Least-Squares Analysis, 511, 548 Lectin, 511, 517 Leisure Activities, 422, 511 Lens, 424, 454, 455, 511, 571 Lentivirus, 511 Leptin, 180, 512 Lethal, 243, 457, 512, 522 Lethargy, 512 Leucine, 75, 512 Leucocyte, 449, 512, 515 Leukemia, 408, 494, 512 Leukocytes, 460, 468, 486, 497, 506, 512, 567 Leukotrienes, 455, 483, 503, 512 Libido, 450, 512 Library Services, 432, 512 Life Expectancy, 373, 512 Ligament, 512, 543 Ligands, 466, 507, 512 Ligase, 512 Ligation, 4, 365, 369, 512 Likelihood Functions, 512, 548 Lincomycin, 470, 512 Linear Models, 512, 548 Linkage Disequilibrium, 513 Lipase, 513, 529 Lipid A, 513, 529 Lipid Peroxidation, 513, 531 Lipophilic, 513 Lipopolysaccharide, 497, 513 Lipoprotein, 77, 372, 483, 497, 513, 514 Lipoprotein Lipase, 513 Lipoprotein(a), 513
Liposome, 513 Lipoxygenase, 455, 512, 513 Lisinopril, 81, 219, 513 Lithium, 235, 453, 513 Liver Cirrhosis, 207, 244, 513 Liver scan, 440, 514, 552 Liver Transplantation, 4, 369, 514 Lobe, 467, 514 Localization, 505, 514 Locomotion, 514, 537 Logistic Models, 514, 548 Longitudinal study, 514 Long-Term Care, 514 Loop, 219, 251, 391, 493, 501, 514 Low vision, 426, 514 Low-density lipoprotein, 483, 513, 514 Lower Body Negative Pressure, 514 Lubricants, 514, 523 Luciferase, 514 Lumbar, 468, 514, 564 Lumen, 454, 485, 514 Lung Transplantation, 515 Lupus, 239, 375, 515, 561 Lymph, 385, 457, 468, 470, 485, 502, 515, 523, 552, 559 Lymph node, 385, 457, 468, 515, 523, 552 Lymphatic, 365, 485, 506, 515, 518, 528, 556, 557, 563 Lymphatic system, 515, 556, 557, 563 Lymphoblastic, 515 Lymphoblasts, 445, 446, 515 Lymphocyte, 453, 515, 516, 517 Lymphoid, 452, 512, 515 Lymphokines, 515 Lymphoma, 408, 515 Lysine, 500, 503, 515, 567 M Macrophage, 515 Macrophage Activation, 515 Macula, 515 Macula Lutea, 515 Macular Degeneration, 207, 426, 515 Magnetic Resonance Angiography, 515 Magnetic Resonance Imaging, 239, 241, 515, 552 Major Histocompatibility Complex, 498, 516 Malabsorption, 408, 516 Malformation, 516 Malignant, 408, 453, 455, 503, 516, 521, 523, 546 Malignant tumor, 516, 521
586 Hypertension
Malnutrition, 177, 448, 456, 516, 521 Mammary, 474, 513, 516 Mandible, 449, 468, 516, 549 Manic, 453, 513, 516 Manifest, 516 Marital Status, 362, 516 Mastication, 516, 566 Matrix metalloproteinase, 516 Meat, 369, 479, 516, 552 Meat Products, 479, 516 Meatus, 516, 569 Mechanoreceptors, 498, 516 Medial, 455, 516, 528, 564 Mediate, 6, 466, 481, 516 Mediator, 82, 516, 554 Medical Records, 4, 517 Medicament, 517 MEDLINE, 6, 403, 407, 409, 517 Medullary, 182, 517 Megaloblastic, 492, 517 Meiosis, 517, 560 Melanin, 509, 517, 535, 567 Melanocytes, 517 Melanoma, 408, 517 Membrane Glycoproteins, 517 Membrane Lipids, 517, 536 Membrane Proteins, 466, 509, 517 Memory, 8, 82, 359, 478, 517 Meninges, 467, 476, 517, 557 Meningioma, 517 Menopause, 207, 344, 517, 533, 539, 540, 542 Menstrual Cycle, 517, 541 Menstruation, 477, 483, 517 Mental Disorders, 259, 517, 541, 544 Mental Health, iv, 259, 402, 405, 518, 541, 544 Mental Processes, 481, 518, 544 Mercury, 491, 518 Mesenchymal, 487, 518 Mesenteric, 518, 539 Mesenteric Arteries, 518 Mesenteric Veins, 518 Mesentery, 518, 534, 557 Meta-Analysis, 518 Metabolic disorder, 479, 496, 518 Metabolite, 480, 492, 518, 540, 541, 546 Metaplasia, 518 Metastasis, 466, 516, 518, 523 Methanol, 518 Methionine, 480, 518, 559 Methyldopa, 220, 393, 518
Metoclopramide, 518 Mibefradil, 519 Microbe, 519, 565 Microbiology, 446, 457, 519 Microcirculation, 499, 513, 519, 537 Microdialysis, 519 Microglia, 456, 519, 520 Microorganism, 471, 519, 571 Micro-organism, 478, 519, 536 Microscopy, 236, 458, 519 Microsomal, 519 Microspheres, 519 Midodrine, 394, 519 Migration, 231, 515, 519 Milliliter, 460, 519 Millimeter, 519 Mineralocorticoid, 226, 519 Miosis, 520 Miotic, 520, 536 Mitosis, 454, 520 Mobilization, 520 Modeling, 482, 520 Modification, 248, 249, 351, 449, 494, 520, 545 Modulator, 520 Molecular Probes, 520 Monitor, 476, 520, 527 Monoamine, 520, 567 Monoamine Oxidase, 520, 567 Monoclonal, 502, 520 Monoclonal antibodies, 520 Monocrotaline, 229, 521 Monocyte, 240, 521 Monogenic, 521 Monotherapy, 179, 521 Morphine, 521, 523, 528 Morphological, 353, 448, 484, 517, 521 Morphology, 499, 515, 521 Motility, 492, 506, 521, 554 Motion Sickness, 521, 523 Motor Activity, 474, 521 Mucinous, 493, 521 Mucosa, 180, 487, 515, 521, 541 Mucus, 521, 567 Multicenter study, 521 Multicystic Dysplastic Kidney, 521 Multiple Myeloma, 334, 521 Multiple sclerosis, 375, 521 Muscle Fibers, 521, 522, 566 Muscle Hypertonia, 521, 524 Muscle Relaxation, 521 Muscular Atrophy, 408, 521
Index 587
Muscular Dystrophies, 483, 521 Musculature, 491, 522 Mustard Gas, 509, 522 Mydriasis, 522 Mydriatic, 480, 522, 535 Myelin, 521, 522 Myelofibrosis, 522 Myocardial Ischemia, 248, 451, 475, 522 Myocardial Reperfusion, 522, 549 Myocardial Reperfusion Injury, 522, 549 Myocardium, 451, 518, 522 Myosin, 462, 522, 566 Myotonic Dystrophy, 408, 522 N Naloxone, 248, 522, 523 Naltrexone, 523 Naphthalenes, 523 Narcosis, 523 Narcotic, 240, 521, 523 Natriuresis, 451, 523 Natriuretic Hormone, 523 Nausea, 385, 438, 452, 453, 454, 493, 503, 523, 544, 568 NCI, 1, 258, 401, 470, 523 Near Drowning, 523 Needs Assessment, 523 Neonatal, 7, 506, 523 Neonatal period, 7, 523 Neoplasia, 408, 523 Neoplasms, 176, 453, 464, 523, 546, 562 Neoplastic, 450, 502, 515, 523 Nephrectomy, 383, 523 Nephritis, 334, 523 Nephrogenic, 524 Nephrologist, 364, 524 Nephron, 495, 510, 524 Nephropathy, 4, 7, 192, 334, 339, 370, 372, 373, 407, 510, 524 Nephrosis, 524 Nephrotic, 334, 524 Nephrotic Syndrome, 334, 524 Nerve Endings, 76, 497, 524, 561 Networks, 524 Neuralgia, 524 Neuroeffector Junction, 524, 526 Neuroendocrine, 524 Neurogenic, 353, 363, 524, 568 Neurologic, 7, 503, 524 Neuromuscular, 191, 445, 524, 526, 549, 568 Neuromuscular Diseases, 191, 524 Neuromuscular Junction, 445, 524, 549
Neuromuscular Junction Diseases, 524, 549 Neuronal, 462, 523, 525 Neurons, 76, 478, 488, 493, 507, 524, 525, 526, 560 Neuropathy, 457, 525 Neuropeptide, 525 Neurophysiology, 478, 525 Neuropsychological Tests, 525 Neurosecretory Systems, 485, 525 Neurosurgeon, 525 Neurotensin, 525 Neurotic, 525, 569 Neutrons, 449, 525, 546 Neutrophil, 240, 525 Nicardipine, 525 Nicotine, 526 Nicotinic Agonists, 526 Nifedipine, 220, 526 Nisoldipine, 382, 394, 526 Nitrendipine, 8, 526 Nitric acid, 526 Nitroglycerin, 250, 369, 509, 526 Nitroprusside, 250, 256, 526 Nonmalignant, 366, 526 Nuclear, 419, 458, 479, 488, 493, 527, 550 Nuclear Medicine, 419, 527 Nuclei, 449, 452, 494, 515, 520, 525, 527, 529, 544 Nucleic acid, 494, 502, 504, 505, 526, 527, 545 Nucleic Acid Hybridization, 502, 527 Nucleotidases, 502, 527 Nursing Care, 527, 532 Nutritive Value, 177, 527 O Occult, 527 Oculi, 527 Oculomotor, 522, 527 Oculomotor Nerve, 522, 527 Odds Ratio, 527, 548 Odour, 455, 527, 568 Oedema, 528, 540 Oliguria, 510, 528 Omega-3 fatty acid, 188, 254, 528 Omentum, 500, 528 Oncogene, 408, 528 Oncogenic, 507, 511, 528 Oocytes, 528 Oophorectomy, 528 Opacity, 478, 528 Open Reading Frames, 511, 528
588 Hypertension
Operon, 528, 549 Opiate, 521, 522, 528 Opioid Peptides, 354, 486, 528 Opium, 521, 528 Opsin, 528, 550, 551 Optic Chiasm, 504, 528, 529 Optic disc, 246, 528 Optic Disk, 474, 479, 515, 529, 531 Optic Nerve, 482, 528, 529, 544, 550, 552 Optic Nerve Diseases, 529, 544 Optic nerve head, 482, 529 Organ Culture, 529, 564 Organ Transplantation, 426, 529 Organelles, 467, 477, 517, 529 Orgasm, 483, 529, 553 Orlistat, 80, 529 Orthostatic, 374, 405, 454, 514, 529 Osmolality, 529 Osmoles, 529 Osmosis, 529 Osmotic, 448, 509, 529, 554 Ossification, 529, 551 Osteoarthritis, 529, 537 Osteodystrophy, 176, 177, 530 Osteoporosis, 359, 421, 488, 530 Ouabain, 530, 558 Outpatient, 7, 238, 240, 530 Ovariectomy, 530 Ovaries, 528, 530, 554 Ovary, 475, 488, 530 Overexpress, 530 Overweight, 176, 177, 185, 254, 363, 438, 530 Ovum, 475, 477, 495, 530, 541, 572 Oxalate, 503, 530 Oxalic Acid, 463, 530 Oxidants, 530 Oxidation, 80, 373, 445, 453, 455, 477, 496, 500, 513, 530, 531 Oxidation-Reduction, 530 Oxidative metabolism, 447, 512, 530 Oxides, 531 Oximetry, 531 Oxygen Consumption, 450, 489, 531, 549 Oxygenase, 531 Oxygenation, 241, 500, 501, 504, 531 Oxygenator, 464, 531 Oxytocin, 531 P Palliative, 531, 563 Palsy, 205, 531
Pancreas, 365, 445, 459, 480, 500, 507, 509, 513, 531, 541, 556, 557, 567 Pancreatic, 408, 465, 531 Pancreatic cancer, 408, 531 Pancreatitis, 531 Panic, 531 Papain, 531 Papilla, 360, 531 Papilledema, 503, 531, 544 Parasite, 531 Parasitic, 531 Parathyroid, 81, 364, 532, 551, 562 Parathyroid Glands, 532, 551 Parathyroid hormone, 364, 532 Parenteral, 486, 532 Parietal, 452, 532, 534, 538 Parietal Lobe, 452, 532 Parotid, 532, 552 Paroxetine, 257, 532 Paroxysmal, 408, 451, 498, 532, 535, 572 Partial remission, 532, 548 Patch, 474, 532 Patent ductus arteriosus, 532 Pathogenesis, 75, 77, 176, 226, 229, 336, 353, 364, 366, 378, 532 Pathologic, 445, 451, 454, 459, 474, 503, 532, 539, 549, 557, 560 Pathologic Processes, 454, 532 Pathologies, 532 Patient Care Management, 334, 532 Patient Compliance, 368, 532 Patient Education, 229, 232, 345, 347, 355, 373, 416, 430, 432, 443, 532 Patient Satisfaction, 532 Pedigree, 533 Pelvic, 533, 543 Pelvis, 445, 506, 514, 530, 533, 545, 568, 569 Penicillin, 452, 533, 569 Penis, 483, 533, 541 Pepsin, 533 Pepsinogen C, 533 Peptic, 226, 533, 553 Peptic Ulcer, 226, 533, 553 Peptic Ulcer Hemorrhage, 533, 553 Peptide Fragments, 533 Peptide Hydrolases, 502, 533 Peptide T, 533 Perception, 533, 552 Perennial, 533, 566 Perforation, 492, 533 Perfusion, 239, 504, 533, 564 Pericarditis, 533
Index 589
Pericardium, 533, 561 Pericytes, 533 Perimenopausal, 533 Perimetry, 534 Perinatal, 82, 234, 506, 534 Perindopril, 534 Perioperative, 534 Peripheral Nervous System, 486, 518, 524, 525, 526, 531, 534, 541, 556, 559 Peripheral Nervous System Diseases, 524, 534 Peripheral Vascular Disease, 534 Peripheral vision, 534, 571 Peristalsis, 481, 534 Peritoneal, 364, 479, 528, 534 Peritoneal Cavity, 528, 534 Peritoneal Dialysis, 364, 479, 534 Peritoneum, 518, 528, 534, 550 Perivascular, 519, 534 Peroxide, 534 Perspiration, 437, 534 Pertussis, 534, 572 PH, 76, 78, 417, 460, 535 Phagocyte, 530, 535 Pharmaceutical Preparations, 467, 488, 494, 535 Pharmacist, 535 Pharmacokinetic, 535 Pharmacologic, 4, 183, 248, 354, 363, 368, 369, 374, 405, 451, 457, 498, 535, 564, 565, 568 Pharmacotherapy, 355, 535 Pharynx, 535, 569 Phenoxybenzamine, 394, 535 Phenyl, 535 Phenylalanine, 221, 535, 567 Phenylephrine, 535 Phenytoin, 463, 535 Phosphates, 535 Phosphodiesterase, 536 Phospholipases, 536, 555 Phospholipids, 490, 513, 517, 536 Phosphoric Monoester Hydrolases, 502, 536 Phosphorous, 536 Phosphorus, 211, 369, 462, 532, 536 Phosphorylate, 536 Phosphorylated, 471, 536 Phosphorylation, 536 Photocoagulation, 471, 536 Phrenic Nerve, 536, 549
Physical Examination, 239, 243, 249, 368, 370, 536 Physical Therapy, 427, 536 Physostigmine, 536 Pigmentation, 536 Pigments, 459, 465, 536, 550 Pilocarpine, 536 Piloerection, 504, 536 Pilot study, 536 Piroxicam, 537 Pituitary Gland, 475, 537 Placenta, 177, 488, 490, 537, 541 Plaque, 451, 537 Plasma, 81, 180, 240, 249, 448, 452, 460, 466, 469, 485, 490, 491, 494, 495, 496, 500, 503, 510, 513, 519, 521, 523, 537, 540, 544, 548, 549, 553, 554, 564 Plasma cells, 452, 521, 537 Plasma protein, 448, 485, 537, 540, 544, 554 Plasmid, 537, 570 Plasmin, 537, 540 Plasminogen, 537 Plasminogen Activators, 537 Plasticity, 537 Platelet Activation, 537, 555 Platelet Aggregation, 450, 487, 504, 526, 538, 542, 563 Platelets, 257, 526, 537, 538, 563 Platinum, 514, 538 Plethysmography, 249, 255, 538 Pleural, 528, 538 Pleural cavity, 528, 538 Pneumonia, 474, 538 Pneumothorax, 413, 538 Poisoning, 462, 482, 493, 508, 518, 523, 538, 553 Polyarteritis Nodosa, 334, 538 Polycystic, 409, 538 Polymerase, 538, 549 Polymorphic, 538 Polymorphism, 538 Polyunsaturated fat, 538, 563 Pons, 458, 461, 492, 538 Porphyria, 538 Porphyrins, 538, 539 Portacaval, 380, 539 Portal Pressure, 369, 539 Portal System, 539 Portal Vein, 245, 518, 539 Portosystemic Shunt, 4, 9, 365, 539 Posterior, 450, 455, 456, 458, 469, 481, 509, 531, 539, 552
590 Hypertension
Posterior chamber, 539 Postmenopausal, 346, 488, 530, 539 Postnatal, 539, 557 Postoperative, 537, 539 Postoperative Complications, 539 Postprandial, 539 Postsynaptic, 524, 525, 539, 555, 561 Post-synaptic, 539, 561 Postural, 539 Potassium Channels, 539 Potentiate, 539 Potentiating, 539 Potentiation, 539, 555 Practice Guidelines, 6, 251, 405, 418, 539 Pravastatin, 540 Prazosin, 221, 394, 540 Precipitating Factors, 466, 498, 540 Preclinical, 360, 540 Predictive factor, 540 Preeclampsia, 77, 207, 208, 365, 412, 540 Pre-Eclampsia, 253, 540 Pre-eclamptic, 483, 540 Prekallikrein, 540 Premenopausal, 540 Prenatal, 366, 484, 540 Prenatal Care, 366, 540 Preoperative, 540 Pressoreceptors, 458, 540 Presynaptic, 524, 525, 540, 560 Presynaptic Terminals, 524, 540 Priapism, 240, 541 Primary Prevention, 236, 252, 361, 541 Probe, 519, 541 Problem-Based Learning, 541 Procainamide, 541 Procaine, 541 Prodrug, 492, 541, 546 Progeny, 541 Progesterone, 541, 558 Prognostic factor, 541 Progressive disease, 541 Proinsulin, 541, 545 Projection, 478, 508, 526, 529, 541, 547 Prolactin, 481, 541 Proline, 74, 471, 503, 542 Promoter, 542 Prone, 181, 182, 254, 542 Propanolol, 542 Prophase, 528, 542, 560 Prophylaxis, 8, 542 Proportional, 250, 529, 542 Propranolol, 221, 456, 542, 564
Prospective Studies, 542 Prospective study, 81, 181, 514, 542 Prostaglandin Endoperoxides, 487, 542, 543, 563 Prostaglandin-Endoperoxide Synthase, 476, 542 Prostaglandins A, 506, 542, 543 Prostaglandins D, 543 Prostaglandins F, 542, 543 Prostaglandins G, 543 Prostaglandins H, 543 Prostate, 176, 359, 386, 408, 459, 533, 543, 553, 567 Protease, 472, 543 Protective Agents, 462, 543 Protein Binding, 543, 564 Protein C, 448, 449, 454, 457, 513, 543, 566, 568 Protein Kinases, 543 Protein S, 362, 409, 459, 494, 543, 551, 562 Proteinuria, 77, 334, 364, 365, 372, 495, 521, 524, 540, 543 Proteoglycans, 458, 489, 543 Proteolytic, 449, 472, 486, 491, 531, 537, 543 Prothrombin, 441, 544, 563 Protocol, 227, 240, 247, 544 Protons, 449, 502, 509, 544, 546 Pseudohypoaldosteronism, 544 Pseudotumor Cerebri, 425, 508, 544 Psychiatric, 517, 544 Psychiatry, 8, 544, 558, 570 Psychic, 470, 512, 517, 544, 553 Psychoactive, 544, 562, 572 Psychology, 227, 354, 355, 357, 481, 544 Psychomotor, 463, 544 Public Health, 364, 374, 405, 419, 544 Public Policy, 403, 544 Pulmonary Alveoli, 504, 544 Pulmonary Circulation, 357, 361, 544 Pulmonary Edema, 413, 468, 510, 544 Pulmonary Veins, 422, 545 Pulmonary Ventilation, 239, 545, 549 Pulsation, 492, 545 Pupil, 469, 474, 480, 520, 522, 545 Purified Insulins, 541, 545 Purines, 545, 554, 572 Purpura, 334, 545 Pyelonephritis, 545 Pyridoxal, 476, 545 Pyridoxal Phosphate, 476, 545 Pyrimidines, 545, 554
Index 591
Q Quality of Life, 233, 426, 545 Quaternary, 545 Quiescent, 545 Quinidine, 545 Quinine, 545 R Racemic, 546 Radiation, 451, 457, 475, 486, 491, 492, 493, 509, 515, 546, 552, 572 Radioactive, 457, 460, 498, 502, 505, 514, 520, 527, 528, 546, 552 Radiography, 412, 451, 467, 474, 546 Radioimmunoassay, 546 Radioimmunotherapy, 546 Radiolabeled, 546 Radiological, 9, 380, 412, 546 Radiology, 350, 412, 527, 546 Radiotherapy, 546 Ramipril, 221, 244, 546 Random Allocation, 546 Randomization, 546 Randomized clinical trial, 546 Randomized Controlled Trials, 6, 547 Rarefaction, 547 Reaction Time, 8, 547 Reactive Oxygen Species, 547 Reagent, 468, 488, 502, 514, 530, 547 Receptor, 75, 76, 78, 79, 81, 178, 179, 211, 226, 231, 255, 257, 368, 370, 386, 446, 453, 468, 469, 481, 488, 497, 525, 533, 546, 547, 554, 555 Receptors, Serotonin, 547, 554 Recombinant, 547, 570 Recombination, 445, 494, 547 Recovery of Function, 547 Rectal, 547 Rectum, 454, 461, 472, 480, 491, 493, 506, 511, 543, 547 Recurrence, 5, 470, 547 Red blood cells, 255, 385, 487, 500, 531, 547, 551 Red Nucleus, 456, 547 Reductase, 182, 186, 540, 547 Refer, 1, 462, 472, 481, 508, 514, 515, 525, 546, 547, 554, 565 Reflex, 547 Reflux, 548 Refraction, 548, 557 Refractory, 9, 79, 368, 483, 548 Regimen, 178, 470, 483, 532, 535, 548 Regression Analysis, 548
Regurgitation, 548 Relative risk, 548 Remission, 547, 548 Renal Artery, 370, 371, 503, 548 Renal Circulation, 460, 548 Renal pelvis, 511, 548 Renal Plasma Flow, 548 Renal tubular, 548 Renin, 74, 81, 180, 232, 249, 253, 342, 351, 364, 370, 451, 463, 510, 548 Reperfusion, 522, 549 Reperfusion Injury, 549 Repressor, 528, 549 Reproductive cells, 495, 501, 549 Research Design, 549 Research Support, 549 Resorption, 549 Respiration, 454, 464, 468, 520, 549 Respiratory distress syndrome, 462, 549 Respiratory Paralysis, 7, 549 Respiratory Physiology, 549, 570 Respiratory System, 415, 448, 549 Restoration, 522, 536, 549, 572 Resuscitation, 4, 549 Retinae, 515, 550 Retinal, 83, 233, 426, 479, 480, 503, 528, 529, 550 Retinal Ganglion Cells, 83, 529, 550 Retinal Hemorrhage, 503, 550 Retinal Neovascularization, 550 Retinal Vein, 550 Retinoblastoma, 408, 550 Retinol, 550, 551 Retinopathy, 4, 208, 373, 435, 479, 550 Retrograde, 508, 550 Retroperitoneal, 446, 550, 571 Retrospective, 550 Retroviral vector, 494, 550 Rhamnose, 530, 550 Rheumatic Diseases, 550 Rheumatism, 550 Rheumatoid, 471, 530, 537, 550 Rheumatoid arthritis, 471, 537, 550 Rhodopsin, 528, 550 Riboflavin, 551 Ribonuclease, 551 Ribonucleoside Diphosphate Reductase, 503, 551 Ribose, 446, 551 Ribosome, 551, 566 Rickets, 551 Rigidity, 508, 537, 551
592 Hypertension
Risk patient, 551 Rod, 470, 551 Rosiglitazone, 249, 551 Rubber, 249, 445, 551 Rural Population, 551 S Salivary, 480, 531, 551, 559 Salivary glands, 480, 551 Saphenous, 474, 551 Saphenous Vein, 474, 551 Saponins, 551, 558 Saralasin, 552 Sarcoidosis, 385, 552 Sarcoplasmic Reticulum, 463, 552 Sarcosine, 552 Satellite, 343, 354, 552 Saturated fat, 176, 367, 552 Scans, 239, 387, 552 Schizoid, 552, 572 Schizophrenia, 454, 552, 572 Schizotypal Personality Disorder, 552, 572 Scimitar Syndrome, 552 Sclera, 469, 473, 474, 552 Scleroderma, 208, 232, 386, 387, 418, 455, 552 Sclerosis, 183, 334, 408, 455, 471, 521, 552 Sclerotherapy, 4, 6, 8, 9, 365, 369, 553 Sebaceous, 509, 553, 571 Sebaceous gland, 509, 553, 571 Secretory, 524, 553, 560 Sedative, 457, 553, 569 Sedentary, 382, 553 Sediment, 553 Sedimentation, 467, 553 Segmental, 334, 491, 495, 553 Segmentation, 553 Segregation, 457, 547, 553 Seizures, 438, 463, 503, 532, 535, 553 Semen, 483, 543, 553 Seminal fluid, 533, 553 Semisynthetic, 464, 470, 553 Senile, 454, 530, 553 Sensor, 553 Sepsis, 553 Septal, 452, 553, 554 Septic, 456, 553 Septicemia, 553 Septum, 553, 554 Septum Pellucidum, 554 Sequela, 554 Sequence Homology, 533, 554 Sequencing, 554
Serine, 476, 554, 567 Serologic, 505, 554 Serotonin, 75, 257, 453, 476, 490, 520, 525, 532, 535, 547, 554, 567 Serous, 485, 554 Serum Albumin, 546, 554 Sex Characteristics, 446, 450, 554, 562 Sex Determination, 408, 554 Sexually Transmitted Diseases, 375, 554 Shock, 502, 554, 566 Shunt, 4, 239, 379, 380, 441, 554 Sibutramine, 80, 554 Signal Transduction, 462, 466, 555 Signs and Symptoms, 238, 538, 548, 555, 568 Skeletal, 248, 450, 470, 509, 521, 522, 545, 552, 555, 556, 566 Skeleton, 445, 490, 510, 542, 555 Skull, 423, 425, 476, 508, 555, 562 Sleep apnea, 555 Small intestine, 468, 469, 482, 501, 504, 508, 510, 555, 567 Smooth muscle, 79, 255, 373, 448, 450, 457, 460, 461, 462, 473, 490, 501, 521, 526, 533, 542, 543, 549, 555, 556, 559, 570 Sneezing, 535, 555 Soaps, 491, 555 Social Class, 555 Social Environment, 545, 555 Social Security, 547, 555 Social Support, 191, 229, 230, 555, 558 Social Work, 240, 364, 555 Sodium Bicarbonate, 556 Sodium Dodecyl Sulfate, 556 Solid tumor, 451, 556 Solitary Nucleus, 457, 556 Solvent, 488, 496, 518, 529, 556 Soma, 556 Somatic, 248, 446, 470, 484, 502, 517, 520, 534, 556, 569 Somatostatin, 8, 369, 556 Sound wave, 250, 473, 556, 568 Soybean Oil, 538, 556 Spasm, 475, 501, 524, 556, 562 Spasmodic, 535, 556 Spatial disorientation, 481, 556 Specialist, 368, 370, 427, 480, 556 Specificity, 447, 455, 462, 557, 564 Spectrometer, 557 Spectrum, 252, 470, 519, 557 Sperm, 450, 469, 495, 501, 549, 553, 557 Sphygmomanometer, 557
Index 593
Spices, 367, 557 Spina bifida, 375, 557 Spinal cord, 456, 461, 467, 468, 469, 493, 517, 524, 525, 534, 541, 547, 549, 557, 560 Spinal Cord Diseases, 549, 557 Spinal Stenosis, 557 Spleen, 366, 385, 450, 515, 552, 557 Splenic Vein, 518, 539, 557 Sporadic, 422, 550, 557 Staging, 552, 557 Stasis, 557 Statistically significant, 557 Steatosis, 490, 557 Steel, 82, 470, 557, 569 Stellate, 557 Stem Cells, 487, 557 Stenosis, 241, 364, 370, 371, 491, 558 Stent, 9, 369, 558 Sterile, 456, 532, 558 Sterility, 506, 558 Steroid, 459, 464, 475, 551, 558 Stimulant, 476, 481, 501, 509, 510, 558, 569 Stimulus, 248, 474, 482, 483, 488, 507, 509, 511, 547, 558, 563 Stool, 472, 506, 511, 558 Stress management, 558 Stricture, 558 Stroma, 509, 558 Strophanthins, 464, 558 Stupor, 512, 523, 558 Styrene, 551, 558 Subacute, 506, 558 Subarachnoid, 492, 498, 558 Subclinical, 506, 553, 558 Subcutaneous, 238, 446, 483, 528, 532, 559, 571 Submandibular, 559 Submaxillary, 486, 559 Subspecies, 556, 559 Substance P, 228, 256, 518, 553, 559 Substrate, 342, 476, 486, 502, 559, 567 Substrate Specificity, 559 Suction, 491, 559 Sudden cardiac death, 559 Sudden death, 79, 559 Sulfates, 556, 559 Sulfur, 489, 518, 559 Sulfuric acid, 559 Sulindac, 559 Superior Cervical Ganglion, 559 Superior vena cava, 461, 559 Superoxide Dismutase, 79, 559
Supine, 559 Supplementation, 183, 254, 559 Support group, 375, 420, 421, 424, 426, 559 Suppression, 383, 475, 559 Suppressive, 559 Suppuration, 560, 571 Suprarenal, 560 Supraspinal, 560 Sural Nerve, 560 Surfactant, 488, 556, 560 Survival Rate, 6, 560 Sweat, 504, 534, 560 Sympatholytics, 560 Sympathomimetic, 481, 487, 509, 527, 560, 567 Symphysis, 468, 543, 560 Symptomatic, 243, 531, 560 Symptomatology, 257, 560 Synapse, 447, 524, 540, 560, 566 Synapsis, 560 Synaptic, 525, 526, 555, 560 Synaptic Transmission, 526, 560 Synaptosomes, 561 Syncope, 208, 561 Synergistic, 541, 561 Synostosis, 561 Systemic, 183, 334, 358, 364, 380, 385, 390, 391, 392, 393, 394, 395, 442, 450, 454, 460, 461, 471, 487, 499, 506, 508, 528, 539, 552, 553, 556, 561, 566, 569 Systemic disease, 553, 561 Systemic lupus erythematosus, 334, 471, 561 Systems Analysis, 561 Systole, 561 Systolic blood pressure, 8, 441, 561 Systolic heart failure, 179, 561 Systolic pressure, 561 T Tachycardia, 408, 481, 561, 565 Tachyphylaxis, 561 Tacrolimus, 561 Tamponade, 365, 561 Tardive, 454, 561 Tear Gases, 509, 561 Telangiectasia, 408, 561 Telencephalon, 458, 467, 562 Temporal, 182, 234, 498, 515, 516, 562 Tendon, 493, 562 Tennis Elbow, 562 Teratogenic, 480, 562 Terbutaline, 562
594 Hypertension
Testis, 488, 562 Testosterone, 547, 562 Tetany, 532, 562 Tetracycline, 482, 562 Tetrahydrocannabinol, 463, 562 Thalamic, 456, 562 Thalamic Diseases, 456, 562 Thalassemia, 458, 562 Thalidomide, 562 Thermal, 232, 235, 481, 525, 563 Thigh, 490, 563 Third Ventricle, 504, 563 Thoracic, 563, 572 Thoracic Surgery, 563 Thorax, 445, 514, 559, 563, 569 Threonine, 533, 554, 563 Threshold, 450, 488, 503, 563 Thrombin, 490, 538, 543, 544, 563 Thrombocytes, 538, 563 Thromboembolism, 563 Thrombolytic, 537, 563 Thrombomodulin, 543, 563 Thromboplastin, 441, 540, 563 Thrombosis, 176, 181, 507, 543, 553, 558, 563 Thromboxanes, 455, 476, 483, 503, 542, 543, 563 Thrombus, 475, 506, 509, 522, 538, 563, 570 Thymus, 505, 515, 563 Thyroid, 504, 508, 532, 563, 564, 567 Thyroid Gland, 504, 532, 564 Thyroid Hormones, 564, 567 Thyrotropin, 564 Thyroxine, 448, 535, 564 Tibial Nerve, 560, 564 Time Management, 558, 564 Timolol, 179, 222, 392, 564 Timolol Maleate, 564 Tinnitus, 544, 564 Tissue Culture, 564 Tissue Distribution, 564 Tolazoline, 564 Tolerance, 446, 496, 564 Tomography, 473, 552, 564 Tonic, 464, 565 Tonicity, 510, 565 Tonometer, 565 Tonometry, 565 Tonus, 565 Tooth Preparation, 446, 565 Torsades de Pointes, 565 Torsion, 506, 565
Toxaemia, 540, 565 Toxicity, 366, 385, 482, 518, 536, 565 Toxicology, 182, 404, 565 Toxin, 485, 564, 565 Trabecular Meshwork, 565 Trace element, 491, 565 Trachea, 461, 511, 535, 563, 564, 565 Tracheostomy, 565 Traction, 236, 470, 565 Transcription Factors, 565 Transduction, 555, 565 Transfection, 459, 494, 566 Transfusion, 239, 240, 566 Translating, 566 Translation, 449, 566 Translocation, 566 Transmitter, 445, 456, 481, 489, 509, 516, 518, 526, 566, 567 Trauma, 385, 459, 531, 547, 566 Trees, 551, 566 Tremor, 564, 566 Triad, 500, 566 Tricuspid Atresia, 474, 566 Tricuspid Valve, 244, 566 Trigeminal, 566 Triglyceride, 504, 566 Trimethaphan, 566 Tropoelastin, 566 Tropomyosin, 566 Troponin, 566 Trypsin, 486, 567 Tryptophan, 471, 554, 567 Tuberous Sclerosis, 408, 567 Tumor marker, 459, 567 Tumor Necrosis Factor, 563, 567 Tumour, 493, 567 Tunica, 485, 521, 567 Tyramine, 189, 520, 567 Tyrosine, 77, 481, 567 U Ubiquitin, 567 Ulcer, 533, 567, 569 Ulcerative colitis, 567 Ultrafiltration, 499, 567 Ultrasonography, 567 Ultrasound test, 244, 568 Unconscious, 442, 451, 478, 504, 568 Unsaturated Fats, 491, 568 Uraemia, 531, 568 Urea, 385, 457, 510, 560, 568 Uremia, 510, 548, 568 Ureter, 548, 568
Index 595
Urethra, 533, 543, 568 Uric, 441, 448, 497, 504, 545, 568 Urinary Retention, 540, 568 Urinary tract, 334, 457, 568 Urinary tract infection, 334, 457, 568 Urinate, 568, 571 Urogenital, 568 Urogenital Diseases, 568 Urokinase, 568 Urologic Diseases, 375, 413, 568 Urology, 371, 568 Ursodeoxycholic Acid, 80, 366, 568 Uterine Contraction, 531, 569 Uterus, 468, 475, 477, 485, 491, 492, 517, 525, 530, 541, 561, 569 V Vaccine, 544, 569 Vacuoles, 485, 529, 569 Vagal, 569 Vagina, 468, 478, 517, 561, 569 Vagus Nerve, 556, 569 Valerian, 192, 569 Valine, 552, 569 Valves, 569 Vanadium, 569 Varices, 3, 6, 8, 365, 380, 407, 487, 569 Varicose, 208, 553, 569 Varicose vein, 553, 569 Vascular Capacitance, 569 Vascular endothelial growth factor, 569 Vasculitis, 334, 531, 538, 569 Vasoactive, 8, 83, 569 Vasoconstrictor Agents, 569, 570 Vasodilatation, 361, 465, 510, 569 Vasodilator Agents, 453, 570 Vasomotor, 488, 570 Vasopressins, 510, 570 Vasopressor, 570 VE, 4, 253, 570 Vector, 566, 570 Vena, 570 Venous blood, 240, 467, 570 Venous Thrombosis, 371, 570 Ventilation, 462, 501, 570 Ventricle, 456, 474, 544, 545, 561, 566, 570 Ventricular Dysfunction, 78, 570 Ventricular fibrillation, 565, 570
Ventricular Function, 570 Ventricular Remodeling, 247, 570 Venules, 460, 463, 485, 519, 570 Verapamil, 223, 348, 395, 571 Vertebrae, 557, 571 Vertebral, 458, 557, 571 Vesicular, 519, 571 Veterinary Medicine, 403, 571 Villous, 469, 571 Viral, 426, 491, 495, 528, 565, 571 Viral Hepatitis, 571 Viral vector, 571 Virilization, 571 Virulence, 565, 571 Virus, 239, 457, 467, 486, 494, 495, 497, 498, 537, 550, 566, 571 Visceral, 457, 534, 569, 571 Visceral Afferents, 457, 569, 571 Visceral fat, 571 Vitreous, 479, 511, 539, 550, 571 Vitreous Body, 550, 571 Vitreous Hemorrhage, 479, 571 Vitro, 230, 460, 494, 500, 505, 561, 564, 571 Vivo, 230, 571 Void, 571 Vomica, 211, 571 W War, 498, 522, 572 Weight Gain, 421, 572 White blood cell, 445, 446, 452, 458, 512, 515, 521, 525, 537, 572 Whooping Cough, 535, 572 Windpipe, 535, 563, 572 Withdrawal, 81, 192, 572 Womb, 569, 572 Wound Healing, 451, 466, 507, 516, 572 X Xanthine, 83, 448, 572 Xanthine Oxidase, 448, 572 Xenobiotics, 572 Xenograft, 452, 572 X-ray, 239, 412, 440, 451, 460, 466, 473, 474, 491, 493, 527, 546, 552, 572 Y Yeasts, 535, 572 Z Zymogen, 543, 572
596 Hypertension
