Table Of ContentARTERIAL AND VENOUS SYSTEMS IN ESSENTIAL HYPERTENSION
DEVELOPMENTS IN
CARDIOVASCULAR MEDICINE
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Hanrath P, Bleifeld W, Souquet, J. eds: Cardiovascular diagnosis by ultrasound. Transesophageal, computerized,
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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.
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Beamish RE, Singal PK, Dhalla NS, eds: Stress and heart disease. 1985. ISBN 0-89838-709-4.
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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.
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Legato MJ, ed: The stressed heart. 1987. ISBN 0-89838-849-X.
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Sideman S, Beyar R, eds: Activation, metabolism and perfusion of the heart. 1987.
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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
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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
