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      Endothelial Dysfunction in Atherosclerosis

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          Abstract

          Endothelial injury or dysfunction has been proposed to be one of the initiating events of atherosclerosis and is associated with an apparent decrease in the production of the vasodilator autacoid nitric oxide (NO). The nature of the endothelial dysfunction resulting in an attenuation of NO-mediated responses is unknown although possibilities include decreased substrate availability, decreased expression of the NO synthase, imbalance between the production of endothelium-derived constricting and relaxing factors, production of an endogenous NO synthase inhibitor and overproduction of oxygen-derived free radicals. While experimental evidence has been provided to support almost all of these possibilities, increased production of superoxide anions within the vascular wall is currently favoured as an explanation for the observed changes in vascular responsiveness and the characteristic loss of the anti-adhesive properties of the endothelium in the early stages of atherosclerosis. The altered ratio of NO/superoxide anion (O<sub>2</sub> production has been proposed to alleviate intrinsic inhibition of the transcription factor NFkB and lead to enhanced expression of adhesion molecules and chemotactic factors at the endothelial surface. The aim of this short review is to summarise recent findings which suggest that an imbalance in the production of NO and O<sub>2</sub> within the vascular wall is one of the earliest events to occur in the atherogenic process.

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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
          1996
          1996
          24 September 2008
          : 33
          : 3
          : 181-194
          Affiliations
          Zentrum der Physiologie, Klinikum der J.W.-Goethe-Universität, Frankfurt/Main, Deutschland
          Article
          159147 J Vasc Res 1996;33:181–194
          10.1159/000159147
          8924517
          © 1996 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: 14
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