Relative androgen sensitivity of the vascular and striated-muscle systems regulating penile erection in rats. 
In this study we sought to compare the androgen sensitivity of the penile vascular erectile system with that of the striated muscles that augment the vascular effectors.  All males were castrated 2 weeks before the experiments.  At the time of castration, all males were implanted SC with a 45-mm testosterone (T)-filled Silastic capsule to maintain reflexive erections in ex copula tests.  Experimental males had the bulbospongiosus (bulbocavernosus and levator ani) and ischiocavernosus muscles removed, while control animals underwent sham muscle excision surgery.  After two baseline penile reflex tests, the T capsules were removed, and the groups were compared for the rate of loss of penile responses over 5 weeks.  After these tests were completed, the T capsules were reimplanted and the two groups were compared for the rate of restoration of penile reflexes.  These tests were conducted at 6, 12, 24, 36, 48, 72, and 96 h after reimplantation of the T capsules.  Our results demonstrated that the vascular effector mechanisms responsible for initiating erections are androgen sensitive.  The effects of T withdrawal and replacement on erection latency and low intensity erections (E1s) were manifested at about the same rate in the vascular and striated muscle effector systems.  In contrast, the restoration of moderate intensity erections (E2s) by T occurred at a faster rate in rats with intact penile muscles.  This result suggests that T was acting on the striated muscle effector systems to augment penile erection during this time, presumably due to the bulbospongiosus muscle exerting greater force on the penile bulb.