The effects of electrical stimulation of hypogastric nerve and sympathetic chain on 'electroerection' (penile erection induced by electrical stimulation of the pelvic nerve) were studied in dogs to clarify the physiological roles that these neural inputs may play in producing and/or maintaining penile erection. As an objective parameter of hemodynamics of the penile circulation, the pressure in the corpus cavernosum of the penis was measured. Hypogastric nerve electrostimulation was performed in 24 dogs who had received pelvic nerve stimulation and, therefore, had 'electroerection'. Ten dogs responded to this procedure with an augmentation of 'electroerection', 10 with an attenuation of 'electroerection', and 4 with no appreciable changes. 4 out of the 10 animals who exhibited an attenuation response were then given an alpha 1-adrenergic blocker (prazosin hydrochloride) prior to the electrical stimulation to evaluate the specificity of the effects of the hypogastric nerve stimulation. In 3 of the 4 dogs the attenuation effect was abolished by this treatment and instead an augmentation effect became evident. Sympathetic chain electrostimulation was performed in 6 dogs with 'electroerection'. When applied to the L4-5 interganglionic segment, it produced a biphasic response which consisted of an initial increase followed by a decrease of the intracorporeal pressure. In contrast, stimulation of the L2-3 interganglionic segment produced a monophasic response consisting of only augmentation of the intracorporeal pressure. These data suggested that there might be two groups of fibers in the hypogastric nerve and sympathetic chain which are functioning antagonistically, and that the anti-erectile neural inputs are mediated primarily by the alpha 1-adrenergic system. To examine the sites of penile vasculature where the innervating hypogastric nerve exerts its effects, electrical pelvic/hypogastric nerve stimulations were performed in dogs in whom the inflow blood circulation to the corpora cavernosa was disrupted by arterial ligation and replaced by a constant saline infusion. It appears that the stimulatory input via the hypogastric nerve caused an increased blood flow into the cavernous space due to vasodilation of the inflow blood vessels, and the inhibitory effect occurred mainly due to relaxation of the draining blood vessels with a resultant increase of the blood outflow from the cavernous space.