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      Reperfusion-Induced Arrhythmias Are Suppressed by Inhibition of the Angiotensin II Type 1 Receptor

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          Abstract

          We examined antiarrhythmic effects of drugs, including renin-angiotensin system (RAS) inhibitors, on reperfusion arrhythmias in rats in vivo. Anesthetized rats were subjected to 5 min of coronary occlusion and 30 min of reperfusion. Arrhythmia scores, calculated as the product of the type of arrhythmia (1 for ventricular tachycardia, 2 for ventricular fibrillation) and its duration (in seconds), were adopted to evaluate the severity of arrhythmias. Reperfusion arrhythmias were suppressed by Na<sup>+</sup>/H<sup>+</sup> exchange inhibitor, Na<sup>+</sup>/Ca<sup>2+</sup> exchange inhibitor and L-type Ca channel antagonist by more than 90%. Angiotensin-converting enzyme inhibitor and angiotensin II (Ang II) type 1 receptor (AT<sub>1</sub>) antagonist also modestly (by 60–70%) but significantly decreased reperfusion arrhythmias. These effects were not reversed by co-administration of bradykinin B<sub>2</sub> receptor antagonist or AT<sub>2</sub> antagonist, respectively. Effects of superoxide dismutase (SOD) were also examined, but SOD proved ineffective. Effects of Na<sup>+</sup>/H<sup>+</sup> exchange inhibitor, Na<sup>+</sup>/Ca<sup>2+</sup> exchange inhibitor and L-type Ca channel antagonist suggest a causative relationship of Ca overload in reperfusion arrhythmias. These transport systems are known to be activated by Ang II. Thus, the antiarrhythmic action of RAS inhibitors might be attributable to the inhibition of the action of Ang II via AT<sub>1</sub>.

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          Most cited references 8

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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2003
                April 2003
                25 April 2003
                : 99
                : 2
                : 61-67
                Affiliations
                Department of Internal Medicine, Fukuoka University School of Medicine, Fukuoka, Japan
                Article
                69722 Cardiology 2003;99:61–67
                10.1159/000069722
                12711879
                © 2003 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
                Figures: 2, Tables: 1, References: 38, Pages: 7
                Categories
                General Cardiology – Basic Science

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