Direct Inhibitory Effects of 17β-Estradiol on hCG-Stimulated cAMP and Testosterone Responses of Canine Testis

The direct effects of 17β-estradiol (E2) on testicular function were investigated using in situ perfusion of canine testis. During perfusion of E2 (10^-8-10^-4M), we measured the concentrations of cAMP, testosterone (T), androstenedione and 5α-dihydrotestosterone (DHT) in the spermatic venous effluent after hCG (500 IU) injection into the spermatic artery.
The cAMP concentration in the spermatic venous effluent was 122 ± 3. 7 (SE) pmoles/ml, increasing after hCG to a peak level of 259.1 ± 33.0 (SE) pmoles/ml at 45 min and decreasing thereafter. T increased gradually from the pretreated level of 12.2 ± 4.4 (SE) mg/ml to 90.9 ± 30.9 (SE) ng/ml at 90 min after hCG injection. Androstenedione production was also stimulated by hCG. Although the pattern of changes of DHT in the venous effluent was similar to that of T, a statistical significant increase was not observed after hCG injection. Continuous infusion with E2 at the concentrations of 10^-8-^-4 M decreased hCG-induced cAMP increase in a dose-dependent fashion. The peak level of cAMP after hCG was shown to be increasingly depleted (50 and 80%) by the increasing doses of 10^-6 and 10^-4 M of exogenous E2. The responses of T and androstenedione were also suppressed by E2 and at 10^-4 M of E2 no increase was observed, although the response of cAMP to hCG remained. These findings indicate that E2 can directly suppress the hCG-stimulated steroidogenesis and cAMP production in in situ canine testis.