help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Journal of Clinical Endocrinology & Metabolism Vol. 68, No. 1 219-222
doi:10.1210/jcem-68-1-219
Copyright © 1989 by the Endocrine Society.
This Article
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 Google Scholar
Google Scholar
Right arrow Articles by KAUFMAN, J. M.
Right arrow Articles by VERMEULEN, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by KAUFMAN, J. M.
Right arrow Articles by VERMEULEN, A.

Lack of Effect of the {alpha}-Adrenergic Agonist Clonidine on Pulsatile Luteinizing Hormone Secretion in a Double Blind Study in Men*

J. M. KAUFMAN and A. VERMEULEN

Department of Endocrinology, University Hospital Ghent B-9000 Gent, Belgium

Address all correspondence and requests for reprints to: Dr. Jean-Marc Kaufman, State University Hospital, Department of Endocrinology, De Pintelaan 185, B-9000-Ghent, Belgium.

This study was designed to evaluate the effects of {alpha}-adrenergic stimulation on the hypothalamic LHRH pulse generator in men. In 10 normal men, venous blood was sampled on 2 occasions at 10-min intervals for 8 h, beginning 30 min after oral administration of either placebo or 0.3 mg clonidine according to a randomized double blind protocol. Compared to placebo, clonidine induced a marked release of GH (P < 0.0001 for response areas under the curve after placebo and clonidine), a fall in systolic and diastolic blood pressure and in heart rate (P < 0.002 for areas under the curve after placebo and clonidine), and feelings of sedation and dry mouth (P < 0.002 and P < 0.05 for areas under the cumulative scores for changes in alertness and salivation, respectively). There was no difference between the results obtained after placebo and clonidine for the mean number of LH pulses [3.3 ± 0.4 (±SE) and 3.3 ± 0.3 pulses/8 h], for the mean amplitude of all LH pulses (3.8 ± 0.4 and 4.1 ± 0.5 IU/L), or for the areas under the LH concentration-time curve (2741 ± 251 and 2728 ± 215 IU/L · min). The lack of effect of clonidine on LH secretion at a dose that effectively induced GH secretion and other centrally mediated effects indicates that the actions of testosterone and opiates to decelerate the frequency of the LHRH pulse generator in men are not mediated by diminished {alpha}-adrenergic stimulation. From these results, taken together with previous data, we conclude that aadrenergic systems do not play a major role in the regulation of episodic LH release in men.

* Presented at the 70th Annual Meeting of The Endocrine Society, New Orleans, LA, June 1988. This work was supported by a grant from the Belgian National Fund for Scientific Research (NFWO).

Received April 5, 1988.







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 © 1989 by The Endocrine Society