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      Role of Alpha-Adrenergic Mechanism in Effects of Morphine on the Hypothalamo-Pituitary-Adrenocortical and Cardiovascular Systems in the Rat

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          Abstract

          The role of α-adrenergic mechanism in the acute effects of morphine in the hypothalamo-pituitary-adrenocortical (HPA) and cardiovascular (CV) systems, and the interrelationship between the HPA and CV responses to α-adrenoceptor antagonists and/or morphine were studied by peripheral administration of prazosin, a selective αi-adrenoceptor antagonist, and yohimbine, a selective α<sub>1</sub>-adrenoceptor antagonist, in conscious, unstressed or ether-stressed rats. The test substances were administered intravenously or intraperitoneally in chronically cannulated or noncannulated rats. In the i.v. experiment, morphine (1 mg/100 g BW) rapidly induced a pronounced bradycardia and a short-lasting fall in blood pressure (BP), followed by a rise in BP, and increased plasma corticosterone concentration. Prazosin (0.5 mg/kg BW) induced a rapid fall in BP and tachycardia, and increased plasma corticosterone concentration. Pretreatment with prazosin did not block the effect of morphine on the CV system, but abolished the morphine-induced increment in plasma corticosterone concentration. Yohimbine (0.5 mg/kg BW) induced a rapid and a subsequent slowly developing rise in BP and tachycardia, and increased plasma corticosterone concentration. Pretreatment with yohimbine did not block the effect of morphine on the CV system nor alter the stimulatory effect of morphine on the secretion of corticosterone. In the intraperitoneal experiment, morphine (2 mg/100 g BW) stimulated the secretion of adrenocorticotropic hormone (ACTH) and corticosterone and prazosin (1 mg/kg BW) stimulated the secretion of corticosterone, but pretreatment with prazosin reduced the morphine-induced increment in plasma corticosterone concentration in unstressed rats. In stressed rats, morphine reduced the stress-induced increment in plasma ACTH and corticosterone concentrations and prazosin also reduced the stress-induced increment in plasma corticosterone concentration. Pretreatment with prazosin did not alter the inhibitory effect of morphine. Taken together with the established concept that morphine acts in the HPA axis primarily at the level of the hypothalamus, the results suggest that: (1) in unstressed rats, morphine acutely stimulates the secretion of corticotropin-releasing factor (CRF) and/or other ACTH secretagogues in the hypothalamus partly through noradrenergic and/or adrenergic pathways: morphine facilitates the secretion of these catecholamines which, in turn, release CRF via stimulation of central α<sub>1</sub>-adrenoceptors, rather than α<sub>2</sub>-adrenoceptors; (2) by contrast, in stressed rats, morphine inhibits the secretion of CRF and/or other ACTH secretagogues partly by attenuating central noradrenergic and/or adrenergic activity presumably via inhibition of release of these catecholamines acting on postsynaptic α<sub>1</sub>-adrenoceptors; (3) the stimulatory effect of morphine on the HPA system under unstressed conditions might be ascribable partly to the morphine-induced CV changes; (4) the morphine-induced initial CV depression is independent of α-adrenergic mechanisms.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1989
          1989
          02 April 2008
          : 49
          : 2
          : 181-190
          Affiliations
          Department of Physiology, School of Medicine, University of California, San Francisco, Calif., USA
          Article
          125112 Neuroendocrinology 1989;49:181–190
          10.1159/000125112
          2542829
          © 1989 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: 10
          Categories
          Original Paper

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