ADRENAL CONTROL OF ERECTILE FUNCTION AND NITRIC-OXIDE SYNTHASE IN THERAT PENIS

Penile erection is a nitric oxide (NO)-mediated process that has been shown to be androgen dependent in rats. Castration reduces the activit y of the penile enzyme involved in NO synthesis, nitric oxide synthase (NOS). To determine whether adrenal androgens and/or corticosteroids contribute to this control, the following groups of Fischer 344 adult male rats (n = 5-7) were studied: 1) intact, 2) castrated, 3) adrenale ctomized alone, 4) castrated/adrenalectomized, 5) castrated/adrenalect omized with aldosterone (1.25 mg/kg, sc) and hydrocortisone (12 mg/kg, sc), 6) castrated/adrenalectomized with dihydrotestosterone (1.2-cm S ILASTIC-brand tubing pellet; Dow Coming, Midland, MI), 7) castrated/ad renalectomized with dehydroepiandrosterone (2-cm tubing), 8) castrated /adrenalectomized with aldosterone (1.25 mg/kg, sc), and 9) castrated/ adrenalectomized with hydrocortisone (12 mg/kg, sc). After 1 week, EFS was applied, and the maximal intracavernosal pressure (MIP) and mean arterial pressure (MAP) were recorded. The MIP/MAP ratio in the adrena lectomized group (0.37) was reduced to values found in the castrated g roup (0.40). The Values in both groups were significantly less than th ose in intact controls (0.75). The most significant reduction in MIP/M AP was seen in the adrenalectomized/castrated group (0.16). Erectile r esponse in animals submitted to adrenalectomy and castration was resto red close to intact values with the administration of hydrocortisone a nd aldosterone (0.63). Similar results were obtained by the administra tion of either of the substances alone (0.56 and 0.67, respectively). Penile NOS activity assayed by the L-arginine/citrulline conversion wa s decreased by 55% in the castrated group compared with that in the in tact group, but was not further reduced in the adrenalectomized/castra ted or adrenalectomized groups. Penile neuronal NOS protein content, e stimated by Western blot, was decreased only in the adrenalectomized/c astrated animals (35%), and endothelial NOS content was not affected. These data suggest that the rat adrenal gland contributes to the maint enance of the erectile mechanism and may affect neuronal NOS content i n the penis in the rat model. The possibility that hypotension may pla y a role in the erectile dysfunction observed in adrenalectomized rats cannot be discarded.