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      Mechanism of Mastoparan-Induced EDRF Release from Pulmonary Artery Endothelial Cells

      ,

      Journal of Vascular Research

      S. Karger AG

      Endothelium, Nitric oxide, EDRF, Mastoparan, Calcium, Pulmonary

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          Abstract

          Mastoparan is a wasp venom peptide that activates G-proteins, certain classes of which are involved in the release of endothelium-derived relaxing factor (EDRF). In the present study, we investigated whether this peptide might be a useful tool with which to elucidate the signal transduction pathways responsible for EDRF release from pulmonary artery endothelium. Mastoparan (10-50 µg/ml) elicited an increase in endothelial cell cytosolic free calcium concentration ([Ca<sup>2+</sup>]<sub>i</sub>) and EDRF release in a concentration-dependent manner. Both effects were dependent on Ca<sup>2+</sup> influx, as they were inhibited by removal of extracellular Ca<sup>2+</sup>. In addition, when endothelial cells were suspended in Ca<sup>2+</sup>-free buffer, mastoparan inhibited ATP-induced increases in [Ca<sup>2+</sup>]<sub>i</sub>, presumably by depleting intracellular Ca<sup>2+</sup> stores. More importantly, mastoparan also caused the release of fura-2 from dye-loaded endothelial cells, unlike ATP, which did not affect fura-2 loss. These data indicate that although mastoparan may act on G-proteins to elicit release of Ca<sup>2+</sup> from intracellular stores, the primary mechanism of action responsible for mastoparan’s ability to elicit EDRF release is an increase in cell membrane permeability followed by an influx of extracellular Ca<sup>2+</sup>.

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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
          1993
          1993
          23 September 2008
          : 30
          : 2
          : 68-72
          Affiliations
          Department of Pharmacology, University of Virginia Health Sciences Center, Charlottesville, Va., USA
          Article
          158977 J Vasc Res 1993;30:68–72
          10.1159/000158977
          8504197
          © 1993 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: 5
          Categories
          Research Paper

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