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      Adrenocorticotropin, Prolactin and Beta-Endorphin Stimulatory Actions of Alpha-2-Adrenoceptor Antagonists

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          Abstract

          We studied the effect of glucocorticoid pretreatment, mediobasal hypothalamus lesion (MBHL) and the interaction between clonidine and yohimbine in male Wistar rats to elucidate the sites and/or mechanisms of endocrine actions of α<sub>2</sub>-antagonists. The pretreatment of 1 mg/kg s.c. dexamethasone for 4 days effectively prevented the stimulatory effect of α<sub>2</sub>-antagonists yohimbine (5 mg/kg i.p.) and CH-38083 (1 mg/kg i.p.) on adrenocorticotropin (ACTH) secretion, while the action of these antagonists on prolactin (PRL) and β-endorphin (βE) remained unchanged. The central (i.c.v.) pretreatment of 5 µg/ rat clonidine failed to antagonize the prolactin (PRL) and βE releasing effect of yohimbine. However, it inhibited the yohimbine-induced ACTH secretion. MBHL resulted in a significant enhancement in basal plasma PRL and β-endorphin (βE) levels. But basal plasma ACTH levels have not been changed. Yohimbine failed to stimulate ACTH secretion in MBH-lesions rats, while PRL and βE response to the yohimbine was maintained in these animals. This study confirms that the α<sub>2</sub>-antagonists stimulate ACTH secretion by a cortico-steroid-sensitive mechanism which is located centrally. In contrast, α<sub>2</sub>-antagonists affect PRL and βE secretion via a corticosteroid-insensitive mechanism located at the periphery, possible within the pituitary gland.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1995
          1995
          09 April 2008
          : 61
          : 2
          : 152-158
          Affiliations
          aInstitute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary; bDepartment of Physiology and Biophysics, Georgetown University School of Medicine, Washington, D.C., USA
          Article
          126835 Neuroendocrinology 1995;61:152–158
          10.1159/000126835
          7753333
          © 1995 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: 7
          Categories
          Corticotropin and Proopiomelanocortin Regulation

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