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      Decreased PO 2 and Rabbit Aortic Smooth Muscle Mechanics

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          Abstract

          Rabbit thoracic aorta was used to determine the effects of decreasing PO<sub>2</sub> on the mechanical properties of contractions in response to norepinephrine (NE) and KC1. Aortae were aerated with 45% O<sub>2</sub>/5% CO<sub>2</sub>/50% N<sub>2</sub> and stimulated with 10 µ M NE or 50 m M KCl. At 5 min of stimulation, 5% CO<sub>2</sub>/95% N<sub>2 </sub>aeration was introduced for 15 min, defined as hypoxia. This time period was previously shown to produce similar decrease in [ATP] in either stimulation condition. Force, stiffness and isotonic shortening velocity were monitored during the initial stimulation, during hypoxia and during re-oxygenation. Hypoxia produced a substantial and rapid decrease in force and a concomitant decrease in stiffness during NE stimulation; delayed and smaller decreases in force and stiffness were observed during KC1 stimulation. The force-stiffness relationship was steeper during KC1 than NE stimulation, and hypoxia did not affect these relationships. Isotonic shortening velocity was significantly depressed by hypoxia during both stimulations although the decrease during KC1 stimulation required a longer time. These data demonstrate that relaxation of an agonist-induced contraction in response to hypoxia results from a decrease in the number of activated crossbridges and not formation of rigor bridges.

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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
          1995
          1995
          24 September 2008
          : 32
          : 5
          : 313-319
          Affiliations
          aBockus Research Institute, Graduate Hospital, Philadelphia, Pa., bDepartment of Physiology, University of Pennsylvania School of Medicine, Philadelphia, Pa., cDepartment of Pharmacology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, N.J., USA
          Article
          159105 J Vasc Res 1995;32:313–319
          10.1159/000159105
          7578799
          © 1995 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: 7
          Categories
          Original Paper

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