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      Interactions of Nitrovasodilators, Atrial Natriuretic Peptide and Endothelium-Derived Nitric Oxide

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          Abstract

          Nitroglycerin (NTG), endothelium-derived relaxing factor (EDRF) and atrial natriuretic peptide (ANP) dilate vessels by a final common pathway (cyclic guanosine monophosphate-dependent mechanism). Thus, these vasodilators may potentially influence the vasodilator properties of each other. We examined whether tolerance to NTG influences vasorelaxation to ANP, EDRF and other nitrovasodilators, isosorbide dinitrate (ISDN) and sodium nitroprusside (SNP). Concentration-response curves for various vasodilators during stable contraction to PGF<sub>2α</sub> were examined before and after the induction of NTG tolerance. Rings exposed to NTG (100 µ M) for 60 min showed marked impairment of vasorelaxation to NTG itself. This NTG tolerance significantly attenuated vasorelaxation to either ISDN, SNP or EDRF stimulated by bradykinin. In contrast, the NTG tolerance did not alter vasorelaxation to either ANP or isoproterenol. The attenuated responses to NTG, ISDN, SNP and bradykinin recovered in a time-dependent manner during the subsequent washout period, suggesting this inhibition is reversible. The denudation of the endothelium significantly sensitized relaxation to NTG but did not change relaxation to ANP. These results suggest that (1) vasorelaxations to nitrovasodilators and EDRF are significantly attenuated by NTG tolerance and (2) ANP-induced vasorelaxation is not affected by exposure to either exogenous nitrovasodilator or endogenous endothelium-derived nitric oxide. ANP may be a potentially beneficial vasodilator in arteries which have developed tolerance to nitrovasodilators.

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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
          : 1
          : 78-85
          Affiliations
          Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Kumamoto, Japan
          Article
          159135 J Vasc Res 1996;33:78–85
          10.1159/000159135
          8603131
          © 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: 8
          Categories
          Research Paper

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