Prazosin is a post synaptic alpha adrenergic blocker effective in hypertension, whose hypotensive effect is unaccompanied by reflex tachycardia or hyperreninemia, nor by other evidence of increased sympathetic activity. We studied the baroreceptor reflex arc as a potential mediator of these effects. Twenty-two essential hypertensive men were treated with prazosin alone versus placebo, and experienced a blood pressure fall (from 114.8 +/- 3.6 down to 101.1 +/- 2.5 mmHg, p less than 0.005) unaccompanied by any change in heart rate, plasma renin activity, or several other indices of sympathetic nervous system activity (plasma dopamine-beta-hydroxylase activity; urinary excretion of free catecholamines and vanillyl mandelic acid; all p less than 0.1). Concomitant with the blood pressure fall, there was a significant depression of baroreflex arc sensitivity, from 11.4 +/- 2.0 ms/mmHg down to 6.6 +/- 1.9 ms/mmHg (p less than 0.05), without an associated change in cardiac vagal inhibition (291.2 +/- 46.2 versus 300.3 +/- 19.2 ms, p greater than 0.1). Baroreflex arc sensitivity depression may in part explain the lack of reflex sympathetic outflow noted during prazosin treatment of hypertension.