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Molecular Pharmacology, Vol 18, 45-48, Copyright © 1980 by the American Society for Pharmacology and Experimental Therapeutics
1 Departments of Pharmacology and Neuropsychiatry, St. Marianna University School of Medicine, Kawasaki, Kanagawa,
213, Japan
Adrenergic stimulation of the cyclic AMP system of the prostate from intact, shamoperated, and castrated rats has been investigated. Castration markedly reduced isoproterenol activation of adenylate cyclase associated with a fall in
-adrenergic receptor sites
in the prostatic membrane. These results imply that a loss in the number of adrenergic
receptors might be a major mechanism responsible for the decreased responsiveness of
the prostatic adenylate cyclase to isoproterenol induced by castration. In addition to the
decreased receptors, 5'-guanylyl-imidodiphosphate (Gpp(NH)p) was without effect on
the cylcase activity and the receptor-ligand affinity in the prostate of castrated rats,
suggesting some defects in GTP-regulating mechanisms on the receptor-adenylate cyclase
complex. Supplementation of testosterone propionate to castrated rats restored the
response to isoproterenol of the enzyme activity and the concentration of adrenergic
receptors to levels at precastration. These findings suggest that endogenous androgens
are involved in maintenance of
-adrenergic receptors linked to the adenylate cyclase
system of the prostatic membrane for the full expression of isoproterenol stimulation.