0
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found

      Involvement of Histamine in the Mediation of the Stress-Induced Release of Alpha-Melanocyte-Stimulating Hormone in Male Rats

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The involvement of histaminergic neurons in the neuroendocrine regulation of the release of the pro-opiomelanocortin-derived peptides adrenocorticotropin (ACTH; anterior pituitary lobe) and α-melanocyte-stimulating hormone (α-MSH; intermediate pituitary lobe) was studied in conscious male rats. Pretreatment with the histamine (HA) synthesis inhibitor (S)-α-fluoromethylhistidine (100 µmol/kg i.p. at -6 h or 400 µmol/kg i.p. at –20 and –6 h) had no effect on basal ACTH release but decreased basal α-MSH release. The two doses of (S)-α-fluoromethylhistidine inhibited by 35 and 50% the ACTH response to 5 min of restraint stress and almost prevented the stress-induced α-MSH release. (S)-α-fiuoromethylhistidine (100 µmol/kg) inhibited the ACTH and α-MSH response to ether stress by 50 and 70%, respectively. Intracerebroventricular administration of the HA metabolism inhibitor SKF 91488 (400 or 800 nmol at-15 min) stimulated basal secretion of ACTH and α-MSH dose-dependently and augmented slightly the restraint- and ether-stress-induced release of ACTH and α-MSH. Intracerebroventricular infusion of the H<sub>1</sub> receptor antagonist mepyramine (0.37 µmol) or the H<sub>2</sub> receptor antagonists cimetidine (0.40 µmol) or ranitidine (0.40 µmol) inhibited or prevented the α-MSH response to intracerebroventricular administration of HA (0.27 µmol), restraint or ether stress. Pretreatment with the dopamine receptor agonist bromocriptine or the β-adrenergic receptor antagonist propranolol inhibited the α-MSH response to HA or stress. The results indicate that hypothalamic histaminergic neurons participate in the neuroendocrine regulation of the pro-opiomelanocortin-derived peptides from the anterior (ACTH) and intermediate (α-MSH) pituitary lobe of male rats. The effect of HA and stress is caused via activation of H<sub>1</sub> and H<sub>2</sub> receptors, and may – concerning the effect on α-MSH secretion – be mediated by tuberohypophysial dopaminergic neurons and peripheral circulating epinephrine.

          Related collections

          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1991
          1991
          07 April 2008
          : 54
          : 6
          : 646-652
          Affiliations
          Department of Medical Physiology C, The Panum Institute, University of Copenhagen, Denmark
          Article
          125974 Neuroendocrinology 1991;54:646–652
          10.1159/000125974
          1664503
          © 1991 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
          Original Paper

          Comments

          Comment on this article