Androgenic regulation of estrogenic action on accessory sex organ smooth muscle.

Our previous research has shown that 4 weeks of daily estrogen treatment, started on the day of castration, resulted in significant growth of the guinea pig seminal vesicle smooth muscle, yet little or no estrogenic effect on muscle tissue weight or DNA content was observed when the treatment was initiated after a 1-month period of castration induced regression. With the hypothesis that castration induced reductions in estrogenic sensitivity were due to alterations in the intracellular fate of estradiol in the muscle, we determined, following the intravenous injection of 3H-estradiol to normal, 24-hour castrates and 1-month castrates, the whole muscle tissue accumulation and subcellular distribution of 3H-estradiol. In the same 3 experimental groups, we also determined, using in vitro exchange assays with 3H-estradiol, the number of estrogen binding sites in both the cytosol and salt (1.2 M KCl) soluble fraction of the crude nuclear-myofibrillar pellet. It was found that the loss of estrogenic sensitivity in the 1-month castrate was not due to a reduction in either whole tissue accumulation, subcellular distribution, cytosol binding or salt-soluble nuclear binding of 3H-estradiol. Restoration of estrogenic responses in muscle DNA content and wet weight was achieved by priming 1-month castrates with 5 daily injections of dihydrotestosterone immediately prior to the onset of estrogen treatment. Shorter periods of androgen priming (e.g., 1, 2 or 3 days) slightly enhanced, but did not completely restore, estrogenic responses in muscle wet weight and DNA content. For estrogen sensitive parameters of muscle growth, such as collagen and RNA content, which were not altered in their response to the estrogen treatment by a 1-month period of castration-induced regression, androgen priming prior to estrogen treatment had no effect. Therefore, testicular androgens regulate selected facets of estrogenic sensitivity in guinea pig seminal vesicle smooth muscle; changes in the muscle cytosol or salt-soluble nuclear myofibrillar estrophiles do not appear to be responsible for the changes in estrogenic sensitivity.