help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by McWilliam, J. R.
Right arrow Articles by Meldrum, B. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McWilliam, J. R.
Right arrow Articles by Meldrum, B. S.

Endocrinology, Vol 112, 254-259, Copyright © 1983 by Endocrine Society

ARTICLES

Noradrenergic regulation of growth hormone secretion in the baboon

JR McWilliam and BS Meldrum

We have investigated the effects of iv administered noradrenergic agonists and antagonists on plasma GH concentration in the adolescent baboon, Papio papio, with the aim of defining the relative roles of adrenergic receptor subtypes (alpha 1, alpha 2, beta 1, and beta 2) in the regulation of GH release. Clonidine (0.02 mg/kg) or UK-14,304 (0.02 mg/kg), potent centrally acting alpha 2 noradrenergic agonists, were infused into 24 animals pretreated with either saline, or selective alpha 1 and alpha 2 noradrenergic antagonists. Both agonists potently augment plasma GH, producing peak levels of 30-60 ng/ml 15 min post infusion. These responses can be prevented by the prior infusion of the alpha 2 antagonist, piperoxane (1.0 mg/kg), but not by the alpha 1 antagonist, prazosin (2.0 mg/kg). Log dose response curves of the 2 agonists demonstrate a greater potency for UK-14,304 vs. clonidine on a molar basis. In animals pretreated with monoamine depleting agents (reserpine and alpha-methyl paratyrosine) the plasma GH response to an infusion of clonidine (0.02 mg/kg) is significantly enhanced (P less than 0.001). Beta-Adrenoreceptor antagonism by propranolol (0.02 or 1.0 mg/kg) or the more selective beta 2-adrenoreceptor antagonist, ICI 118,551 (0.02-1.0 mg/kg), results in a rapid and significant (P less than 0.01) increase in plasma GH. The beta 1-antagonist, practolol (0.2- 2.0 mg/kg), does not alter plasma GH levels. It is proposed that in the baboon, noradrenaline acts on alpha 2-noradrenergic receptors to stimulate GH release and on beta 2-noradrenergic receptors to inhibit GH release.


This article has been cited by other articles:


Home page
 EndocrinologyHome page
T. Thomas, F. Gori, T. C. Spelsberg, S. Khosla, B. L. Riggs, and C. A. Conover
Response of Bipotential Human Marrow Stromal Cells to Insulin-Like Growth Factors: Effect on Binding Protein Production, Proliferation, and Commitment to Osteoblasts and Adipocytes
Endocrinology, November 1, 1999; 140(11): 5036 - 5044.
[Abstract] [Full Text]

Home page
 Endocr. Rev.Home page
A. Giustina and J. D. Veldhuis
Pathophysiology of the Neuroregulation of Growth Hormone Secretion in Experimental Animals and the Human
Endocr. Rev., December 1, 1998; 19(6): 717 - 797.
[Abstract] [Full Text]

Home page
 J PsychopharmacolHome page
F. Grossman, H. K. Manji, and W. Z. Potter
Platelet {alpha}2-adrenoreceptors in depression: a critical examination
J Psychopharmacol, January 1, 1993; 7(1_suppl): 4 - 18.
[Abstract] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1983 by The Endocrine Society