Cyclic adenosine monophosphate (cAMP) does not mediate the stimulatory action of norepinephrine on testosterone production by the testis of the golden hamster

Abstract

The role of cAMP in mediating the stimulatory effects of norepinephrine (NE) on testosterone (T) production by hamster testes in vitro was examined using tissue from both gonadally active and gonadally regressed hamsters. As expected from our previous studies, the NE-induced increase in T accumulation in this system was prevented by alpha-adrenoreceptor antagonist prazosin, but not by beta-adrenoreceptor antagonist propranolol. In incubations of regressed testes from short photoperiod-exposed hamsters, NE stimulated accumulation of cAMP in media and tissue. These effects were prevented by propranolol but not by prazosin. In incubations of active testes from long photoperiod-exposed animals, NE stimulated cAMP in the media but not in the tissue, and potentiated the effect of hCG on the accumulation of cAMP only in tissue. When added to incubations with NE and hCG, propranolol, but not prazosin, reduced cAMP levels in media and tissue. Thus, functional alpha- and beta-adrenoreceptors are present in active and regressed testes and can be activated by NE. NE stimulates cAMP production via its action at the beta-receptors and T production via its action at the alpha-receptors. These results imply that cAMP does not mediate the stimulatory action of NE on T production in hamster testes.