+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found

      G Proteins and Endothelium-Dependent Relaxations

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Endothelial cells control the tone of the underlying smooth muscle by releasing relaxing factors (nitric oxide, NO, prostacyclin and endothelium-derived hyperpolarizing factor). G proteins couple a number of endothelial cell receptors to the activation of NO synthase. Pertussis toxin selectively ADP-ribosy-lates certain G proteins (mainly G<sub>i</sub>). In the porcine coronary artery, pertussis toxin inhibits the release of NO evoked by certain (serotonin, α<sub>2</sub>-adrenergic agonists, leukotrienes, thrombin), but not all, (bradykinin, adenosine diphosphate) endothelium-dependent vasodilators. This suggests that both G<sub>i</sub> and G<sub>q </sub>proteins can couple receptor activation to the increase in endothelial Ca<sup>2+</sup> concentration required to stimulate NO synthase. In arteries with regenerated endothelium and in cultured endothelial cells, the release of NO evoked by pertussis-toxin-sensitive mechanisms is severely reduced or absent, while the response to other endothelium-dependent agonists is normal. To judge from experiments with cultured endothelial cells, the curtailment in pertussis-toxin-sensitive release of NO is due to an abnormal function rather than a reduced presence of G<sub>i</sub> proteins, or a reduced sensitivity of the cell membrane receptor. The selective impairment of G<sub>i</sub> proteins in regenerated endothelial cells predisposes the blood vessel wall to vasospasm and to the initiation of the atherosclerotic process.

          Related collections

          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          24 September 2008
          : 34
          : 3
          : 175-185
          aINSERM, Hôpital Lariboisière, Paris et bInstitut de Recherches Internationales Servier, Courbevoie, France
          159221 J Vasc Res 1997;34:175–185
          © 1997 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: 11


          Comment on this article