The effects of bromocriptine administered by peripheral or central routes were studied in neurogenic hypertensive dogs. The acute hypertension was elicited by deafferentation (sino-aortic denervation). Intravenous (0,15 to 0,30 mg/kg) bromocriptine induced an important decrease in blood pressure of the debuffered dog (Fig. I). Bromocriptine reduced the arrhythmia induced by deafferentiation, but not the tachycardia of the debuffered dog (Table I). Bromocriptine was active by intracisternal route, at a dose (0,15 mg/kg) effective by intravenous route (Fig. 2). This antihypertensive effect of bromocriptine was also observed in debuffered dogs with binding of both vertebral and carotid arteries (i.e. when an effect of the drug on central structures was ruled out) (Fig. 3), and was suppressed by pretreatment with haloperidol, a dopaminergic antagonist (Fig. 4). These results imply that the mechanism underlying the hypotensive effect of bromocriptine is dopamine receptor stimulation; we consider that an effect on central nervous structures does not play a significant role in the hypotensive effect of this drug following acute intravenous administration in the dog.