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      Effect of Aldostetone and Salt Intake on Renal and Pressor Actions of Angiotensin

      , , ,

      Nephron

      S. Karger AG

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          Abstract

          In man and dogs, natriuresis is produced by angiotensin in some states associated with hyperaldosteronism more readily than in the normal state. In the rat, aldosterone has been reported to augment renin induced natriuresis. To investigate these unexpected findings, 0.100 µg/kg/min of angiotensin was administered to normal, aldosterone treated and salt-depleted dogs. Natriuresis occurred in some normal dogs, but in none of the others. It was concluded that aldosterone does not augment and may inhibit natriuresis induced in dogs by angiotensin. Other aspects of renal function were also studied. Angiotensin was found less likely to induce natriuresis during a water diuresis than during an osmotic diuresis. The pressor response to angiotensin was significantly reduced by salt-depletion, but was not affected by aldosterone infusion. A salt load slightly increased the pressor response to angiotensin. In a comparative study, the pressor response to norepinephrine was found to be unaffected by salt-depletion. Data from 92 experiments confirmed the reported inverse correlation between mean control blood pressure and the pressor response to angiotensin. A similar, although much weaker, correlation existed for the pressor response to norepinephrine. Possible explanations for this phenomenon are discussed and the influence on it of variations in salt intake described.

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          Author and article information

          Journal
          NEF
          Nephron
          10.1159/issn.1660-8151
          Nephron
          S. Karger AG
          1660-8151
          2235-3186
          1966
          1966
          26 November 2008
          : 3
          : 6
          : 329-343
          Affiliations
          Department of Medicine, Georgetown University School of Medicine, and Renal and Electrolyte Division, Georgetown University Hospital, Washington, D.C.
          Article
          179550 Nephron 1966;3:329–343
          10.1159/000179550
          4289495
          © 1966 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
          Pages: 15
          Categories
          Paper

          Cardiovascular Medicine, Nephrology

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