Mechanism of Potassium Relaxation of Arterial Muscle

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Abstract

Strips of arterial muscle were prepared from rat tail and femoral arteries and dog mesenteric arteries. All muscles developed a contracture slowly when exposed to a potassium-free solution, but relaxed rapidly when potassium was added to the bath to give a concentration as low as 0.1 mM. The slow contracture is caused by norepinephrine release from intrinsic nerve endings, but the rapid relaxation occurs while the norepinephrine concentration is still high. Contractions produced by exogenous norepinephrine or serotonin in a potassium-free bath were also made to relax by the addition of potassium. After several minutes these relaxations reversed abruptly and spontaneously to return to their original level of contraction. The rapid relaxation was found to be due to an electrogenic transport mechanism which caused hyperpolarization within several seconds after the addition of potassium. This hyperpolarization is believed to be caused by electrogenic ion transport since it exceeded the expected membrane potential based on the potential calculated from potassium concentrations, ER. Hyperpolarization declined within 5–15 min, allowing contraction to redevelop. Ouabain was found to prevent both the 1 Supported by USPHS NIH grants HL-03756, HL-14388, HL-16328, and NS-10558. 2 Recipient of Research Career Development award HL-00073 from the National Institutes of Health.

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Journal

Journal ID (publisher-id): JVR

Journal ID (nlm-ta): J Vasc Res

Journal ID (doi): 10.1159/issn.1018-1172

Title: Journal of Vascular Research

Publisher: S. Karger AG

ISSN (Print): 1018-1172

ISSN (Electronic): 1423-0135

Publication date Subscription-year: 1977

Publication date (Print): 1977

Publication date (Electronic): 18 September 2008

Volume: 14

Issue: 5

Pages: 261-276

Affiliations

Departments of Physiology and Pharmacology, University of Michigan, Ann Arbor, Mich., and Department of Pharmacology and the Cardiovascular Center, University of Iowa, Iowa City, Iowa

Article

Publisher ID: 158133 Other ID: Blood Vessels 1977;14:261–276

DOI: 10.1159/000158133

SO-VID: 2e1cd607-eb4d-45cd-90b9-ea60d40abf35

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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.

History

Date received : 25 October 1976

Date accepted : 07 January 1977

Page count

Pages: 16

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