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      Downregulation of Endothelin B Receptors in Cardiomyopathic Hamsters

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          Abstract

          The mechanisms responsible for abnormal fluid retention in congestive heart failure (CHF) are unclear. Studies were conducted to elucidate how endothelin (ET) may contribute to salt and water retention. Cardiomyopathic (CM) hamsters with moderate heart failure were employed for in vivo and in vitro trials. Clearance methods were used to compare the level of renal function in CM hamsters and control animals. Radioligand binding studies were also performed to determine ET receptor distribution in the inner medullary collecting ducts. CM hamsters exhibited an attenuated response to ANF infusion (FE<sub>Na</sub>: 2.7 ± 0.5 vs. 5.9 ± 0.8%, p < 0.01; FE<sub>H2</sub>O: 1.7 ± 0.3 vs. 3.2 ± 0.4%, p < 0.01; U<sub>cGMP</sub>: 11.2 ± 2.3 vs. 16.6 ± 2.0 pmol/min, p < 0.05) and a decrease in total ET receptor density (532 ± 77 vs. 959 ± 154 fmol/mg protein, p < 0.005). Particularly ET<sub>B</sub> receptors were significantly reduced (214 ± 26 vs. 483 ± 88 fmol/mg protein, p < 0.003). Enalapril therapy simultaneously restored the natriuretic and diuretic effects of ANF and ET receptor density in the diseased animals. These studies suggest that the renin-angiotensin-aldosterone system and ET hormonal system act together, via ET<sub>B</sub> receptor downregulation, to promote the abnormal fluid retention observed in CHF.

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          Most cited references 2

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          Influence of congestive heart failure on endothelin levels and receptors in rabbits.

          Congestive heart failure, both in man and in animals is associated with an increased plasma level of endothelin. To investigate further the potential role of the endothelin system, we designed a study to determine the effect of experimental congestive heart failure (CHF) on plasma and tissue immunoreactive-endothelin (irET) and on the density and affinity of endothelin-1 receptors in the heart and kidney. For this purpose, CHF was induced in rabbits by combined aortic valvular insufficiency and stenosis. When CHF was established, plasma and tissue irET levels were measured by radioimmunoassay and density and affinity of endothelin-1 receptors were measured by binding assay on tissue homogenates. Compared to control rabbits, plasma irET was significantly elevated in rabbits with CHF [1.04 +/- 0.15 vs. 0.04 +/- 0.01 fmol/ml, P < 0.001]. Tissue irET concentrations in ventricles and kidney were roughly 4 orders of magnitude higher than plasma concentrations. CHF decreased the tissue irET levels in left ventricle and kidney by 32 and 46%, respectively (P < 0.01), whereas CHF increased it by 58% in the right ventricle (P < 0.005). The density of ET-1 receptors was decreased in the right and left ventricles and in kidneys by 26, 36, and 61%, respectively (P < 0.05). Receptor affinity remained unchanged in response to CHF in both ventricles, whereas it increased in kidney [Kd (pM); 154 +/- 17 vs. 99 +/- 9, P < 0.01]. Thus, this study demonstrates that experimental CHF is not only characterized by elevated plasma irET levels but also by a decrease in tissue irET concentrations in the left ventricle and kidney, and by a down-regulation of ET-1 receptors both in the heart and kidney. Functional consequences of these changes need to be determined.
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            Interaction among atrial natriuretic factor (ANF), vasopressin, and renal nerves in terms of renal responses in rats

             Kaushik Patel (1991)
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              Author and article information

              Journal
              CRD
              Cardiology
              10.1159/issn.0008-6312
              Cardiology
              S. Karger AG
              0008-6312
              1421-9751
              1998
              March 1998
              16 March 1998
              : 89
              : 3
              : 195-201
              Affiliations
              a Department of Medicine, University of British Columbia, Vancouver Hospital and Health Sciences Centre, Koerner Pavilion, Vancouver, B.C., Canada; b Show Chwan Memorial Hospital, Changhua, Taiwan, ROC
              Article
              6787 Cardiology 1998;89:195–201
              10.1159/000006787
              9570434
              © 1998 S. Karger AG, Basel

              Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

              Page count
              Figures: 3, Tables: 2, References: 29, Pages: 7
              Categories
              General Cardiology, Basic Science

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