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      Interaction of Antihypertensive Drugs with Anti-Inflammatory Drugs

      Cardiology

      S. Karger AG

      Enalapril, Nifedipine-GITS, Blood pressure, Nonsteroidal anti-inflammatory drugs, Antihypertensive drugs, Indomethacin

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          Abstract

          Nonsteroidal anti-inflammatory drugs (NSAIDs) can induce an increase in blood pressure (BP) and may potentially reduce the efficacy of several antihypertensive drugs. Probably the main mechanism of action is inhibition of prostaglandin (PG) synthesis since NSAIDs have higher propensity to increase BP as the regulation of BP (and renal function) is more PG-dependent and to interact with drugs (diuretics, β-blockers and ACE inhibitors) that may act through the increase of PG formation. In contrast, NSAIDs do not interact with calcium antagonists and central acting drugs which actions are apparently unrelated with renal/extrarenal production of PG. It has been claimed that inhibition of natriuretic PGs could explain the pressure effects of NSAIDs in treated hypertensive patients, but sodium retention may be not the single explanation for such an interaction. We found that despite indomethacin produced sodium retention after being added either to enalapril or nifedipine-GITS, it only attenuated (by 45%) the antihypertensive effects of enalapril. In alternative, since PG enhances vasodilatation and attenuates vasoconstrictor influences, some NSAIDs may counteract the PG-dependent vasodilatory tone in renal and extrarenal vascular beds that mediate the antihypertensive action of some drugs. Thus, since calcium antagonists are probably not affected by NSAIDs, they may be preferable to drugs like diuretics, β-blockers and ACE inhibitors for the treatment of high blood pressure control in hypertensive patients who are clinically suitable for NSAIDs therapy.

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          Author and article information

          Journal
          CRD
          Cardiology
          10.1159/issn.0008-6312
          Cardiology
          S. Karger AG
          978-3-8055-6620-9
          978-3-318-01632-1
          0008-6312
          1421-9751
          1997
          1997
          19 November 2008
          : 88
          : Suppl 3
          : 47-51
          Affiliations
          Unidade de Farmacologia Clinica da Faculdade de Medicina do Porto, Portugal
          Article
          177507 Cardiology 1997;88:47–51
          10.1159/000177507
          9397294
          © 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.

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          Pages: 5
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