ARTERIAL AND VENOUS SYSTEMS IN ESSENTIAL HYPERTENSION DEVELOPMENTS IN CARDIOVASCULAR MEDICINE Recent volumes Hanrath P, Bleifeld W, Souquet, J. eds: Cardiovascular diagnosis by ultrasound. Transesophageal, computerized, contrast, Doppler echocardiography. 1982. ISBN 90-247-2692-1. Roelandt J, ed: The practice of M-mode and two-dimensional echocardiography. 1983. ISBN 90-247-2745-6. Meyer J, Schweizer P, Erbel R, eds: Advances in noninvasive cardiology. 1983. ISBN 0-89838-576-8. Morganroth J, Moore EN, eds: Sudden cardiac death and congestive heart failure: Diagnosis and treatment. 1983. ISBN 0-89838-580-6. Perry HM, ed: Lifelong management of hypertension. 1983. ISBN 0-89838-582-2. Jaffe EA, ed: Biology of endothelial cells. 1984. ISBN 0-89838-587-3. Surawicz B, Reddy CP, Prystowsky EN, eds: Tachycardias. 1984. ISBN 0-89838-588-1. Spencer MP, ed: Cardiac Doppler diagnosis. 1983. ISBN 0-89838-591-1. Villarreal H, Sambhi MP, eds: Topics in pathophysiology of hypertension. 1984. ISBN 0-89838-595-4. Messerli FH, ed: Cardiovascular disease in the elderly. 1984. ISBN 0-89838-596-2. Simoons ML, Reiber JHC, eds: Nuclear imaging in clinical cardiology. 1984. ISBN 0-89838-599-7. Ter Keurs HEDJ, Schipperheyn JJ, eds: Cardiac left ventricular hypertrophy. 1983. ISBN 0-89838-612-8. Sperelakis N, ed: Physiology and pathophysiology of the heart. 1984. ISBN 0-89838-615-2. Messerli FH, ed: Kidney in essential hypertension. 1984. ISBN 0-89838-616-0. Sambhi MP, ed: Fundamental fault in hypertension. 1984. ISBN 0-89838-638-1. Marchesi C, ed: Ambulatory monitoring: Cardiovascular system and allied applications. 1984. ISBN 0-89838-642-X. Kupper W, MacAlpin RN, Bleifeld W, eds: Coronary tone in ischemic heart disease. 1984. ISBN 0-89838-646-2. Sperelakis N, Caulfield JB, eds: Calcium antagonists: Mechanisms of action on cardiac muscle and vascular smooth muscle. 1984. ISBN 0-89838-655-1. Godfraind T, Herman AS, Wellens D, eds: Calcium entry blockers in cardiovascular and cerebral dysfunctions. 1984. ISBN 0-89838-658-6. Morganroth J, Moore EN, eds: Interventions in the acute phase of myocardial infarction. 1984. ISBN 0-89838-659-4. Abel FL, Newman WH, eds: Functional aspects of the normal, hypertrophied, and failing heart. 1984. ISBN 0-89838-665-9. Sideman S, Beyar R, eds: Simulation and imaging of the cardiac system. 1985. ISBN 0-89838-687-X. Van der Wall E, Lie KI, eds: Recent views on hypertrophic cardiomyopathy. 1985. ISBN 0-89838-694-2. Beamish RE, Singal PK, Dhalla NS, eds: Stress and heart disease. 1985. ISBN 0-89838-709-4. Beamish RE, Panagio V, Dhalla NS, eds: Pathogenesis of stress-induced hean disease. 1985. ISBN 0-89838-710-8. Morganroth J, Moore EN, eds: Cardiac arrhythmias. 1985. ISBN 0-89838-716-7. Mathes E, ed: Secondary prevention in coronary artery disease and myocardial infarction. 1985. ISBN 0-89838-736-1. lowell Stone H, Weglicki WB, eds: Pathology of cardiovascular injury. 1985. ISBN 0-89838-743-4. Meyer J, Erbel R, Rupprecht HJ, eds: Improvement of myocardial perfusion. 1985. ISBN 0-89838-748-5. Reiber JHC, Serruys PW, Slager CJ: Quantitative coronary and left ventricular cineangiography. 1986. ISBN 0-89838-760-4. Fagard RH, Bekaert IE, cds: Spons cardiology. 1986. ISBN 0-89838-782-5. Reiber JHC, Serruys PW, eds: State of the an in quantitative coronary arteriography. 1986. ISBN 0-89838-804-X. Roelandt J, ed: Color Doppler Flow Imaging. 1986. ISBN 0-89838-806-6. Van der Wall EE, ed: Noninvasive imaging of cardiac metabolism. 1986. ISBN 0-89838-812-0. Liebman J, Plonsey R, Rudy Y, eds: Pediatric and fundamental electrocardiography. 1986. ISBN 0-89838-815-5. Hilger HH, Hombach V, Rashkind WJ, eds: Invasive cardiovascular therapy. 1987. ISBN 0-89838-818-X Serruys PW, Meester GT, eds: Coronary angioplasty: a controlled model for ischemia. 1986. ISBN 0-89838-819-8. Tooke JE, Smaje LH: Clinical investigation of the microcirculation. 1986. ISBN 0-89838-819-8. Van Dam RTh, Van Oosterom A, eds: Electrocardiographic body surface mapping. 1986. ISBN 0-89838-834-1. Spencer MP, ed: Ultrasonic diagnosis of cerebrovascular disease. 1987. ISBN 0-89838-836-8. Legato MJ, ed: The stressed heart. 1987. ISBN 0-89838-849-X. Roelandt J, ed: Digital techniques in echocardiography. 1987. ISBN 0-89838-861-9. Sideman S, Beyar R, eds: Activation, metabolism and perfusion of the heart. 1987. ISBN 0-89838-871-6. Safar ME et aI., cds: Arterial and venous systems in essential hypertension. 1987. ISBN 0-89838-857-0. ARTERIAL AND VENOUS SYSTEMS IN ESSENTIAL HYPERTENSION Editor: M.E. SAFAR Diagnostic Center, Department oj Interna! Medicine Hopita! Broussais, Paris, France Associate Editors: G.M. LONDON, A.CH. SIMON and Y.A. WEISS 1987 MARTINUS NIJHOFF PUBLISHERS 1IIr... a member of the KLUWER ACADEMIC PUBLISHERS GROUP 1111 DORDRECHT I BOSTON I LANCASTER ..... Distributors for the United States and Canada: Kluwer Academic Publishers, P.O. Box 358, Accord Station, Hingham, MA 02018-0358, USA for the UK and Ireland: Kluwer Academic Publishers, MTP Press Limited, Falcon House, Queen Square, Lancaster LAI lRN, UK for all other countries: Kluwer Academic Publishers Group, Distribution Center, P.O. Box 322, 3300 AH Dordrecht, The Netherlands Library of Congress Cataloging in Publication Data Arterial and venous systems in essential hypertension. (Developments in cardiovascular medicine) Includes index. 1. Essential hypertension--Etiology. 2. Physiology, Pathological. 3. Hemodynamics. 4. Cardiovascular system. I. Safar, Michel. II. Series. [DNLM: 1. Cardiovascular'System--physiopathology. 2. Hyper- tension--complications. W1 DE997VME / WG 340 A7828] RC685.A725 1987 616.1'32 86-31256 ISBN-13: 978-94-010-7983-9 e-ISBN-13: 978-94-009-3303-3 DOl: 10.1007/978-94-009-3303-3 Copyright © 1987 by Martinus Nijhoff Publishers, Dordrecht. Softcover reprint of the hardcover 1s t edition 1987 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, mechanical, photocopying, recording, or otherwise, without the prior written permission of the publishers, Martinus Nijhoff Publishers, P.O. Box 163, 3300 AD Dordrecht, The Netherlands. Preface The hemodynamic mechanisms of hypertension are often limited to the study of three dominant parameters: blood pressure, cardiac output and vascular resis- tance. Accordingly, the development of hypertension is usually analyzed in terms of a 'struggle' between cardiac output and vascular resistance, resulting in the classical pattern of normal cardiac output and increased vascular resistance, thus indicating a reduction in the caliber of small arteries. However, during the past years, the clinical management of hypertension has largely modified these simple views. While an adequate control of blood pressure may be obtained with antihypertensive drugs, arterial complications may occur, involving mainly the coronary circulation and suggesting that several parts of the cardiovascular system are altered in hypertension. Indeed, disturbances in the arterial and the venous system had already been noticed in animal hypertension. The basic assumption in this book is that the overall cardiovascular system is involved in the mechanisms of the elevated blood pressure in patients with hypertension: not only the heart and small arteries, but also the large arteries and the venous system. For that reason, the following points are emphasized. First, the cardiovascular system in hypertension must be studied not only in terms of steady flow but also by taking into account the pulsatile components of the heart and the arterial systems. Second, arterial and venous compliances are altered in hypertension and probably reflect intrinsic alterations of the vascular wall. Third, such abnormalities suppose a geometrical redesign of the cardiovascular system, and the structural and the functional components are therefore critical for the understanding of hypertension. Finally, regional blood flows are more important than cardiac output itself for the description of the complications of hypertensive vascular disease. Despite (or due to) the striking remodelling of the cardiovascular system observed in hypertension, it is important to recognize that the principal function of this system, i.e. to maintain an adequate blood flow for the metabolic needs of the tissues, is largely preserved during an important part of the life. Thus an adequate analysis of hypertension requires the description of auto-regulatory VI mechanisms contributing to maintain flow within normal ranges. Of course, such mechanisms are operating in untreated hypertensives, but they are also important to evaluate following antihypertensive treatment. Indeed, each antihypertensive agent is expected to be characterized by a specific mechanism of action, a prerequisite which is in opposition with the apparently non-specific geometrical redesign of the overall cardiovascular system described in patients with essential hypertension. Clearly, the relationships between antihypertensive agents and remodelling of the cardiovascular system following treatment is a key point in the future for a better understanding of cardiovascular morbidity and mortality in patients treated for hypertension. M.E. Safar G.M. London A.Ch. Simon Y.A. Weiss Table of contents Preface v Part I - Small arteries and the concept of resistance Hemodynamic basis for the concept of resistance and impedance in hyper- tension 3 M.F. O'Rourke Structural component of vascular resistance in hypertension 21 B. Folkow Baroreflex mechanisms and the high pressure system in hypertension 37 E.M. Krieger Part II - Low pressure system and the concept of venous distensibility Venous compliance in essential hypertension 53 G.M. London and M.E. Safar Functional and structural components of reduced forearm venous disten- sibility in human hypertension 67 G. Simon Cardiac mechanoreceptors in hypertension 81 A.L. Mark Venous system, extracellular fluid volume and the kidney in essential hypertension 95 G.M. London and M.E. Safar Part III - Large vessels and the concept of arterial compliance Systolic hypertension in the elderly 105 E.D. Frohlich and F.H. Messerli Large arteries in borderline and sustained essential hypertension 115 A. Simon and J. Levenson VIII Pulse wave velocity and hypertension 133 A.P. Avolio Renin-angiotensin system and arterial wall in hypertension 153 V.l. Dzau Part W - Regional circulations The coronary circulation in hypertensive left ventricular hypertrophy 167 P.A. Wicker and R.C. Tarazit Carotido-cerebral circulation in patients with sustained essential hypertension 181 M.E. Safar, St. Laurent and l.A. Bouthier Renal circulation in essential hypertension 197 P.W. de Leeuw and W.H. Birkenhiiger Hepato-splanchnic circulation in human hypertension 211 Y.A. Weiss, G.M. London and M.E. Safar Part V - Forearm circulation as a model for the study of hypertension Methods for investigation of forearm blood flow 223 B.1. Levy The contribution of alpha-1 and alpha-2-adrenoceptor mediated vasoconstriction in essential hypertension as assessed by forearm venous occlusion plethysmography 233 P. Bolli, W. Kiowski and F.R. Buhler Beta-adrenergic receptors and the forearm circulation 253 P. van Brummelen and P.C. Chang Converting enzyme inhibitors and hypertensive large arteries 261 A. Simon and l. Levenson Calcium entry blockers and the forearm arterial bed 273 B.F. Robinson Cations and the forearm circulation in hypertensive humans 285 A. Takeshita and T. Imaizumi Conclusion Homeostatic mechanisms and structural modifications of the cardiovascular system in essential hypertension 303 M.E. Safar List of contributors 321 Part I Small arteries and the concept of resistance Hemodynamic basis for the concept of resistance and impedance in hypertension MICHAEL F. O'ROURKE Hypertension is caused by increased resistance to flow in peripheral vessels. This was appreciated by Bright [1] in 1827 as the probable cause of cardiac hypertrophy in patients with chronic nephritis' ... that it so affects the minute and capillary circulation, as to render greater action necessary to force the blood through the distant subdivisions of the vascular system.' This point of view was emphasised by Sutton and by Gull [2], who in a lecture at Guy's Hospital, London in 1872 observed 'It is always dangerous to rest in a narrow pathology; and I believe that to be a narrow pathology which is satisfied with what you now see before me on this table. In this glass you see a much hypertrophied heart and a very contracted kidney. This specimen is classical. It was, I believe, put up under Dr Bright's own direction and with a view of showing that the wasting of the kidney was the cause of the thickening of the heart. I cannot but look upon it with veneration, but not with conviction. I think, with all deference to so great an authority, that the systemic capillaries, and had it been possible, the entire man, should have been included in this vase; then we should have had, I believe, a truer view of the causation of the cardiac hypertrophy and of disease of the kidney.' Marey in Paris [3] developed the first sphygmograph for measuring arterial pressure in man. This was refined in London by Mahomed (Fig. 1) who must be credited with the first description of the syndrome of essential hypertension [4]. 'My first contention is that high pressure is a constant condition in the circulation of some individuals and that this condition is a symptom of a certain constitution or diathesis' , and further - 'These persons appear to pass through life pretty much as others do and generally do not suffer from high blood pressures, except in their petty ailments upon which it imprints itself ... As age advances the enemy gains ascession of strength ... the individual has now passed forty years, perhaps fifty years of age, his lungs begin to degenerate, he has a cough in the winter time, but by his pulse you will know him ... Alternatively headache, vertigo, epistasis, a passing paralysis, a more severe apoplectic seizure and then the final blow.' Referring to etiology, Mahomed wrote 'What has been the cause in one case may be the result in the other; thus general disorder may cause high blood pressure