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      Effects of Angiotensin II on Canine and Porcine Coronary Epicardial and Resistance Arteries

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          Abstract

          Coronary resistance arteriolar diameter importantly regulates myocardial blood flow, and is influenced by circulating neurohumoral agents. Angiotensin II (A-II) is a circulating polypeptide that is chronically elevated in heart failure and serves as a potent peripheral vasoconstrictor agent. However, its effects on isolated coronary resistance arterioles is relatively unknown. We compared the vasomotor effects of A-II on coronary epicardial and resistance arterioles in vitro from both the canine and porcine heart in order to determine the effects of A-II in different vascular beds and species. Epicardial rings were studied under isometric recording conditions, while resistance arterioles (50–150 µm) were studied in vitro using a video imaging system to record diameter. A-II, whether applied to passively distended or preconstricted porcine resistance arterioles, did not cause vasoconstriction when applied as a bolus or as cumulative doses. In preconstricted canine resistance arterioles, A-II elicited dose-dependent vasodilation (EC<sub>50</sub> = 0.2 n M) . In passively distended canine arterioles, high concentrations of A-II (0.1 µ M)applied as a bolus elicited transient vasoconstriction in 28% of the vessels studied. In large epicardial rings, A-II was a weak vasoconstrictor, with greater potency in canine arteries compared to porcine arteries. In canine arteries, vasoconstriction to A-II was augmented after incubation with indomethacin. In contrast to the findings in canine arteries, the A-II vasoconstrictor response in porcine coronary arteries was decreased after incubation with indomethacin or removal of the endothelium. Thus, A-II elicits the release of a vasodilator prostanoid in epicardial canine coronary arteries and a vasoconstrictor prostanoid in porcine vessels which modulate the vasomotor action of A-II. Receptor binding assays to compare A-II receptors in resistance arterioles and epicardial arteries showed that porcine arterioles possessed significantly more membrane receptors for A-II than porcine epicardial vessels, whereas there was no difference between canine epicardial and arteriolar A-II receptor densities. In conclusion, A-II exerted complex actions on both large epicardial vessels and resistance arterioles, with significant differences between species. A-II was a weak vasoconstrictor in both porcine and canine epicardial vessels. The net vasomotor response was the result of interactions between vasoactive prostanoids and direct smooth muscle vasoconstrictor effects on the coronary artery. A-II was a potent vasodilator of canine, but not porcine, resistance arterioles, and in some vessels elicited transient vasoconstriction at high A-II concentrations. Despite the presence of A-II receptors, in porcine resistance arterioles A-II had no vasomotor effects in either passively distended or preconstricted arterioles.

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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
          1994
          1994
          23 September 2008
          : 31
          : 6
          : 338-346
          Affiliations
          Departments of Medicine and Physiology, College of Medicine, and The Dalton Cardiovascular Research Center, University of Missouri, and Harry S. Truman Memorial Veterans Administration Hospital, Columbia, Mo., USA
          Article
          159062 J Vasc Res 1994;31:338–346
          10.1159/000159062
          7986958
          © 1994 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: 9
          Categories
          Research Paper

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