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      Depression of Contractions of Rabbit Aorta and Guinea Pig Vena cava by Mesudipine and Other Slow Channel Blockers

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          Abstract

          The effects of several drugs having Ca<sup>++</sup>-antagonistic and vasodilating properties were compared in arterial and venous smooth muscles. Developed force (phasic component) was recorded from isolated rings (about 2 mm wide) of blood vessel wall taken from rabbit aorta or guinea pig inferior vena cava. The vascular smooth muscle (VSM) was stimulated to contract for a sustained period by elevating the extracellular K<sup>+</sup> concentration ([K]<sub>o</sub>) to 100 mM or by exposure to norepinephrine (NE). All drugs depressed the K<sup>+</sup>-induced contractures in a dose-dependent manner between 10-9 and 10–5 M. The order of potency in aorta was: mesudipine = verapamil > diltiazem > nifedipine. Of the three drugs studied in vena cava, the order of potency was: mesudipine > verapamil > bepridil. It is concluded that, in both preparations of arterial and venous VSM, mesudipine is the most potent inhibitor of K<sup>+</sup>-induced contractions. Aortic contractions to 10<sup>-7</sup> M NE were depressed at concentrations of Ca<sup>++</sup> antagonists 2 or 3 orders of magnitude less than those needed to depress contractions to 10–5 M NE. The NE-induced contractions were depressed by the drugs to about the same extent as the K<sup>+</sup>-induced contractions when 10<sup>-7</sup> M NE was used, but were depressed to a much smaller extent when 10–5 M NE was used. This may reflect the involvement of intra-cellular Ca<sup>++</sup> storage sites in contractions induced by high NE concentrations. It is likely that these drugs depress and block Ca<sup>++</sup> influx through the cell membrane.

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          Author and article information

          Journal
          JVR
          J Vasc Res
          10.1159/issn.1018-1172
          Journal of Vascular Research
          S. Karger AG
          1018-1172
          1423-0135
          1983
          1983
          19 September 2008
          : 20
          : 4
          : 172-183
          Affiliations
          Department of Physiology, University of Virginia School of Medicine, Charlottesville, Va., USA
          Article
          158471 Blood Vessels 1983;20:172–183
          10.1159/000158471
          © 1983 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: 12
          Categories
          Research Paper

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