The Renal Papilla and Hypertension PDF
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The Renal Papilla and Hypertension The Renal Papilla and Hypertension Edited by Anil K. MandaI, M.D., F.A.C.P. Veterans Administration Medical Center and University of Oklahoma College of Medicine Oklahoma City, Oklahoma and Sven-Olof Bohman, M.D. Karolinska Institute Stockholm, Sweden PLENUM MEDICAL BOOK COMPANY New York and London Library of Congress Cataloging in Publication Data Main entry under title: The Renal papilla and hypertension. Includes bibliographical references and index. 1. Renal hypertension. 2. Renal papilla. I. MandaI, Anil K. II. Bohman, Sven Olof. [DNLM: 1. Hypertension. 2. Kidney medulla. WG340 R393] RC918.R38R46 616.6'1 80-15989 ISBN 978-1-4684-8117-4 ISBN 978-1-4684-811 5-0 (eBook) DOl 10.1007/978-1-4684-8115-0 © 1980 Plenum Publishing Corporation Softcover reprint of the hardcover 1s t edition 1980 227 West 17th Street, New York, N.Y. 10011 Plenum Medical Book Company is an imprint of Plenum Pu blishing Corporation All rights reserved No part of this book may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the Publisher This book is dedicated to our beloved wives and children for their gracious cooperation, which encouraged us in our venture. This book was facilitated in large part through the support of the Medical Research Service of the Veterans Administration, Washington, D. C., and by the Medical Service, Veterans Administration Medical Center, and the Department of Medicine, University of Oklahoma at Oklahoma City, Oklahoma. Contributors SVEN-OLOF BOHMAN • Department of Pathology, Karolinska Institute, Huddinge Hospital, S-141 86 Huddinge, Sweden INGE NORBY BOJESEN • Institute of Experimental Hormone Research, University of Copenhagen, DK-2100 Copenhagen, Denmark MUKUL C. GANGULI • Hypertension Section, Department of Internal Medicine, University of Minnesota Hospital and School of Medicine, Minneapolis, Minnesota 55455 CATHERINE LIMAS • Department of Pathology, Veterans Administration Hospital, and Departments of Laboratory Medicine and Pathology, University of Minnesota School of Medicine, Minneapolis, Minnesota 55455 ANIL K. MANDAL • Department of Medicine, Veterans Administration Medical Center and University of Oklahoma College of Medicine, Oklahoma City, Oklahoma 73104 BASAB K. MOOKERJEE • State University of New York at Buffalo, Buffalo, New York 14215, and Medical Research Service, Veterans Administration Medical Center, Buffalo, New York 14218 ROBERT C. MUEHRCKE • Department of Medicine, West Suburban Hos pital, Oak Park, Illinois 60302 E. E. MUIRHEAD • University of Tennessee Center for the Health Sciences and Baptist Memorial Hospital, Memphis, Tennessee 38146 JOHN A. NORDQUIST • Renal Electron Microscopy Laboratory, Veterans Administration Medical Center, Oklahoma City, Oklahoma 73104 ix x CONTRIBUTORS RAM V. PATAK • University of Kansas Medical Center, Kansas City, Kansas 66103, and Medical Research Service, Veterans Administration Medical Center, Kansas City, Missouri 64128 J. A. PITCOCK • University of Tennessee Center for the Health Sciences and Baptist Memorial Hospital, Memphis, Tennessee 38146 WOLFGANG SIESS • Department of Internal Medicine, University Hos pital, 0-8000 Munich 2, West Germany DINKO susie • Institute for Medical Research, 1101 Belgrade, Yugoslavia LOUIS TOBIAN • Hypertension Division, University of Minnesota College of Medicine, Minneapolis, Minnesota 55455 PETER C. WEBER • Department of Internal Medicine, University Hos pital, 0-8000 Munich 2, West Germany RANDALL MARK ZUSMAN • Harvard Medical School, Boston, Massa chusetts 02115, and Cardiac and Hypertension Units, Medical Services, Massachusetts General Hospital, Boston, Massachusetts 02114 Foreword LOUIS TOBIAN There are many reasons for suspecting that the medulla of the kidney is involved in the pathogenesis of hypertension. Although our present knowledge does not permit the assignment of a precise and exact role for the medulla, there are so many indications of its involvement that this is an appropriate time for the subject to be thoroughly reviewed, as Drs. MandaI and Bohman have done in this volume. The involvement of the renal medulla in hypertension was first strongly indicated by the studies of Eric Muirhead. Studying renoprival hyperten sion, he demonstrated that the injection of extracts of renal medulla could prevent this type of hypertension in the dog, rabbit, and rat. Subsequently, a number of experiments showed that implants of renal medulla could not only prevent renoprival hypertension but also greatly reduce the level of blood pressure in Goldblatt hypertension in the rat and rabbit. It was later noted that the majority of the surviving cells in these medullary implants were interstitial cells. Pitcock and Muirhead were able to culture these interstitial cells, and implants of the cultured cells lowered blood pressure in renoprival hypertension and Goldblatt hypertension, particularly in the rat. We were able to confirm these general observations by employing implants of medulla in "postsalt" hypertension. The medullary implants did indeed bring the blood pressure down. The belief that the implants themselves were the effective agent was strengthened even further by the finding that when they were removed, their antihypertensive effect would disappear and the blood pressure would rise again. The interstitial cells secrete some interesting substances with vasoactive properties. They have definitely been shown to secrete prostaglandins E2 and F2", which of course are very powerful vasoactive agents, and they also LOUIS TOBIAN • Hypertension Division, University of Minnesota College of Medicine, Minneapolis, Minnesota 55455. xi xii LOUIS TOBIAN secrete a neutral lipid material with strong antihypertensive properties. Moreover, another cell in the renal medulla-the collecting duct cell-also has a rich supply of the enzyme that can convert arachidonic acid into prostaglandins. There are thus two types of cells in the renal medulla that are able to synthesize prostaglandins, making the renal medUlla one of the tissues in the body with the richest supply of prostaglandin cyclooxygenase, equaled only by the seminal vesicles themselves. One can therefore look upon the renal medulla as potentially a very active prostaglandin factory. The renal medulla also contains the collecting ducts, which, as the last bit of renal tubule that the urine passes through before emerging into the renal pelvis, have "the last word" with regard to the ultimate excretion of sodium in the urine. Since sodium handling is so intimately involved with the process of hypertension, this particular medullary structure could be of pivotal importance in the hypertensive process from the sodium standpoint alone. Of course, the ascending limb of the loop of Henle also has an extremely active sodium transport system, and this provides the driving force for the countercurrent multiplier system that produces a concentration gradient for NaCI and urea from the tip of the papilla toward the cortex. The very high concentration of N aCI and urea in the papilla is a key ele ment in the conservation of body water. It is now quite definitely known that the prostaglandins have a pro found influence on the concentration of NaCl in the papilla of the kidney. The administration of prostaglandin synthesis inhibitors, such as indo methacin or meclofenamate, can cause a doubling of the sodium concentra tion in the renal papilla. It is thought that this is primarily the result of enhancement of sodium transport out of the ascending limb and the collect ing tubules or ducts after a profound inhibition of prostaglandin synthesis. These are two more examples in which the level of prostaglandin E2 in the papilla and the level of sodium in the papilla appear to go in opposite direc tions. This may turn out to be a common physiological relationship and indicates that prostaglandin levels have a very profound governing influence on the concentration of N aCI in the papilla. One might question what the concentrations of N a and Cl in the papilla have to do with hypertension. Hrst of all, such concentrations would influence the conservation of water in the body. Furthermore, we have observed repeatedly that all forms of experimental hypertension appear to be characterized by an abnormally low concentration of sodium in the papilla. The precise reason for the relationship between the sodium concentration in the renal papilla and the presence of hypertension has not been clearly elucidated, but the low sodium concentration in this region appears to be a part of the general hypertensive process. An alteration in prostaglandin content may be related to this lowering of papillary sodium concentration. Moreover, in earlier studies, it was noted that the number of FOREWORD xiii lipid granules in the cytoplasm of the interstitial cells was also greatly reduced, and that this reduction correlated very strongly with the reduction of sodium concentration in the renal papilla. This general picture of low lipid granules in the interstitial cells and low sodium concentration in the papilla was observed in four distinct forms of experimental hypertension. It has also been pointed out by Moffat that the descending vasa recta are invested with smooth muscle cells and could therefore undergo vaso constriction or vasodilation. Originally, in an effort to study the process of autoregulation in a papilla from a hypertensive rat, the plasma flow to the. renal papilla was measured in various types of experimental rat hyperten sion. It was found that all forms of experimental rat hypertension could be characterized by reduced plasma flow to the renal papilla, even though the flow to virtually every other organ was at normal levels, implying a dispro portionate amount of vasoconstriction in the vessels supplying the papilla. This would suggest that the circulation to the papilla was involved in the hypertensive diathesis to a greater extent than was the circulation to all other vascular beds. This conclusion is suggested by the fact that the papillary vascular resistance increased enough to actually reduce blood flow, whereas in all other vascular beds the resistance also increases, but not sufficiently to actually bring blood flow to lower than normal levels. One can thus find a myriad of abnormalities in the renal papilla in various forms of experimental hypertension. These findings suggest a definite involvement of the renal papilla in the hypertensive process and imply that a number of papillary functions are distinctly abnormal during hypertension.
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