|
|
||||||||
Biology of Reproduction, Vol 30, 416-422, Copyright © 1984 by Society for the Study of Reproduction
ARTICLES |
R Collu, W Gibb and JR Ducharme
Immobilization stress applied for 6 h induced, in adult male rats, a rise of epinephrine (E) and norepinephrine (NE) plasma levels and a decrease of baseline plasma testosterone (T) values and of human chorionic gonadotropin (hCG)-induced T response. Treatment of the animals for 5 weeks with guanethidine (G), a sympathetic neuron toxic agent, significantly decreased E and NE responses to stress and partly antagonized the inhibitory effects exerted by immobilization on T biosynthesis. Adrenalectomy totally suppressed circulating E and reduced the stress-induced NE increase while partly antagonizing the inhibitory effects exerted on T biosynthesis. Combined G and adrenalectomy treatments totally suppressed plasma E and NE, and completely blocked the effects of immobilization on T levels. Treatment of the animals with the alpha 1-adrenergic blocker, prazosin, and the beta 1-adrenergic blocker, metoprolol, did not modify the effects of stress on T biosynthesis. Treatment with propranolol or with butoxamine, a nonspecific beta- and a specific beta 2-adrenergic receptor blocker, respectively, antagonized the testicular hyposensitivity to hCG induced by stress. Stress- or treatment-induced changes of plasma luteinizing hormone (LH) and hCG levels were not consistently correlated with plasma T modifications. These findings suggest that at least part of the inhibitory effects of immobilization stress on T biosynthesis is exerted by catecholamines through a beta 2- adrenergic receptor.
This article has been cited by other articles:
![]() |
R. Yirmiya, I. Goshen, A. Bajayo, T. Kreisel, S. Feldman, J. Tam, V. Trembovler, V. Csernus, E. Shohami, and I. Bab From the Cover: Depression induces bone loss through stimulation of the sympathetic nervous system PNAS, November 7, 2006; 103(45): 16876 - 16881. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |