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      Electrophysiological Basis of Arteriolar Vasomotion in vivo

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          Abstract

          We tested the hypothesis that cyclic changes in membrane potential (E<sub>m</sub>) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters. Diameter oscillations (∼3 min<sup>–1</sup>) were preceded (∼3 s) by oscillations in E<sub>m</sub> of smooth muscle cells (SMC) and endothelial cells (EC). Oscillations in E<sub>m</sub> were resolved into six phases: (1) a period (6 ± 2 s) at the most negative E<sub>m</sub> observed during vasomotion (–46 ± 2 mV) correlating (r = 0.87, p < 0.01) with time (8 ± 2 s) at the largest diameter observed during vasomotion (41 ± 2 µm); (2) a slow depolarization (1.8 ± 0.2 mV s<sup>–1</sup>) with no diameter change; (3) a fast (9.1 ± 0.8 mV s<sup>–1</sup>) depolarization (to –28 ± 2 mV) and constriction; (4) a transient partial repolarization (3–4 mV); (5) a sustained (5 ± 1 s) depolarization (–28 ± 2 mV) correlating (r = 0.78, p < 0.01) with time (3 ± 1 s) at the smallest diameter (27 ± 2 µm) during vasomotion; (6) a slow repolarization (2.5 ± 0.2 mV s<sup>–1</sup>) and relaxation. The absolute change in E<sub>m</sub> correlated (r = 0.60, p < 0.01) with the most negative E<sub>m</sub>. Sodium nitroprusside or nifedipine caused sustained hyperpolarization and dilation, whereas tetraethylammonium or elevated PO<sub>2</sub> caused sustained depolarization and constriction. We suggest that vasomotion in vivo reflects spontaneous, cyclic changes in E<sub>m</sub> of SMC and EC corresponding with cation fluxes across plasma membranes.

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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
          2000
          December 2000
          10 January 2001
          : 37
          : 6
          : 568-575
          Affiliations
          aJohn B. Pierce Laboratory and bDepartment of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Conn., USA; cDepartment of Human Physiology, School of Medicine, Flinders University of South Australia, Adelaide, Australia
          Article
          54090 J Vasc Res 2000;37:568–575
          10.1159/000054090
          11146411
          © 2000 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: 7, References: 27, Pages: 8
          Categories
          Research Paper

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