Previous studies from this laboratory have demonstrated that penile erection in the rat is androgen dependent: 1 wk after castration, there was a significant decline in the magnitude of the intracavernosal pressure (CCP) response during erection induced by stimulation of the autonomic ganglion controlling penile blood flow. The response was altered by vasoactive drugs and appeared to involve nitric oxide synthesis. These earlier studies, however, did not identify the site of androgenic action or the mechanism by which the androgens act. The findings reported here show that even in long-term-castrated animals (up to 7 wk), there remains a rise in CCP in response to ganglionic stimulation, demonstrating that there is an androgen-independent as well as an androgen-dependent portion of the erectile response. Other results show a linear relationship between systemic blood pressure and CCP during erection, although in castrated animals without androgen replacement, the CCP responds less to changes in the systemic pressure than in intact or testosterone-treated animals. This finding could signify a reduced blood inflow and/or an increased blood outflow during erection in the castrated rats. Further studies partially explained the lower erectile pressure by demonstrating that the rate of outflow from the cavernosal spaces was greater in castrated rats than in animals with normal androgen levels. Taken together, these findings show that androgens act to maintain both the inflow and the outflow of blood from the cavernous spaces during erection.