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      Mobilization of Extracellularly Bound Ca 2+ during High K + and Norepinephrine Stimulation of the Rabbit Aorta

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          Abstract

          The effects of α-adrenergic stimulation and high K<sup>+</sup>-induced membrane depolarization on <sup>45</sup>Ca<sup>2+</sup> uptake and tension generation in the rabbit aorta were investigated. Tension and unidirectional <sup>45</sup>Ca<sup>2+</sup> uptake were increased by both stimulants. Moreover, this ‘steady-state’ uptake remained elevated for as long as the stimulants were present. When tissues were preincu-bated in <sup>45</sup>Ca<sup>2+</sup>-containing PSS prior to the Ne or high K<sup>+</sup> challenge the resulting Ca<sup>2+</sup> uptake showed an ‘initial burst’ of uptake which was not observed in the ‘steady-state’ experiments. The magnitude of the ‘initial burst’ increased with time displaying a t<sub>½</sub> for exchange of 1.25 min for both high K<sup>+</sup> and Ne, suggesting that this Ca<sup>2+</sup> source is shared by both stimulants. The ‘initial burst’ became Ca<sup>2+</sup> saturated when [Ca<sup>2+</sup>]<sub>o</sub> was between 0.5 and 1.5 mM, was enhanced by <sup>45</sup>Ca<sup>2+</sup> preincubation in a solution of lowered ionic strength and was inhibited (∼70%) by D600 (5 × 10<sup>–6</sup> M). In contrast, the ‘steady-state’ uptake was linearly dependent on [Ca<sup>2+</sup>]<sub>o</sub> up to 6.4 mM, was 90% inhibited by 5 × 10<sup>–6</sup> M D600 and was unaffected by lowered ionic strength. It is concluded that the properties displayed by the Ca<sup>2+</sup> source responsible for the ‘initial burst’ and ‘steady-state’ uptake suggest that they are of distinct origin; the ‘initial burst’ being derived from a bound extracellular Ca<sup>2+</sup> pool and the ‘steady-state’ uptake resulting from the uptake of free Ca<sup>2+</sup> dissolved in the extracellular space.

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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
          1985
          1985
          23 September 2008
          : 22
          : 5
          : 234-243
          Affiliations
          Department of Pharmacology, University of Miami Medical School, Miami, Fla., USA
          Article
          158607 Blood Vessels 1985;22:234–243
          10.1159/000158607
          © 1985 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: 10
          Categories
          Research Paper

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