+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found

      Decreased Activity of the Sodium-Calcium Exchanger in Tail Artery of Stroke-Prone Spontaneously Hypertensive Rats

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          The ability of the Na-Ca exchanger to modify vascular relaxation was studied in rings isolated from tail arteries of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY). The arteries were contracted with norepinephrine (NE) 1µ M and after stabilization they were transferred to a Ca-free physiological salt solution still in presence of NE. The time to 50% relaxation (T-50) in these conditions was significantly greater in SHRSP (78 ± 7 s) than in WKY (50 ± 7 s). When the calcium pump was stopped with vanadate (VAN), the Ca uptake by the sarcoplasmic reticulum with ryanodine (RY) and the Na-Ca exchanger with a Na-free PSS, the relaxation was slowed (T-50 increased to 198 ± 16 s in SHRSP and to 162 ± 14 s in WKY). Releasing the Na-Ca exchanger only (i.e. still with VAN and RY but with normal Na in the bath) the T-50 for relaxation in Ca-free PSS was, in WKY, nearly as fast as in control conditions (54 ± 8 s). However, the Na-Ca exchanger in SHRSP was not so effective, and the T-50 for relaxation was slower than in control conditions (122 ± 10 s). We conclude that the activity of the Na-Ca exchanger is depressed in tail arteries of SHRSP. This abnormality in resistance vessels, would contribute to the enhanced vascular tone present in hypertension.

          Related collections

          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          23 September 2008
          : 27
          : 2-5
          : 197-201
          Department of Physiology, University of Michigan, Ann Arbor, Mich., USA
          158810 Blood Vessels 1990;27:197–201
          © 1990 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: 5
          Mechanisms of Vasodilatation


          Comment on this article