Neuroendocrinology
Original Paper
Involvement of Histamine in the Mediation of the Stress-Induced Release of Alpha-Melanocyte-Stimulating Hormone in Male RatsKnigge U. · Matzen S. · Hannibal T. · Jørgensen H. · Warberg J.Department of Medical Physiology C, The Panum Institute, University of Copenhagen, Denmark
|
|
Log in to MyKarger to check if you already have access to this content.
KAB
Buy a Karger Article Bundle (KAB) and profit from a discount!
If you would like to redeem your KAB credit, please log in.
Save over 20% compared to the individual article price.
Article / Publication Details
Received: January 15, 1991
Accepted: May 21, 1991
Published online: April 07, 2008
Issue release date: 1991
Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 0
ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)
For additional information: https://www.karger.com/NEN
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 H1 receptor antagonist mepyramine (0.37 µmol) or the H2 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 H1 and H2 receptors, and may – concerning the effect on α-MSH secretion – be mediated by tuberohypophysial dopaminergic neurons and peripheral circulating epinephrine.
© 1991 S. Karger AG, Basel
Related Articles:
Article / Publication Details
Received: January 15, 1991
Accepted: May 21, 1991
Published online: April 07, 2008
Issue release date: 1991
Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 0
ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)
For additional information: https://www.karger.com/NEN
Copyright / Drug Dosage / Disclaimer
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.
Get Permission
PubMed ID
