Pressor responses to intraventricularly administered (IVT) angiotensin II (AII) were markedly potentiated by IVT phentolamine (50, 100 or 200 ug/min for 30 min), not altered by tolazoline (140 ug/min for 30 min) and significantly reduced by phenoxybenzamine (100 ug/min for 30 min). Phentolamine, IVT, also produced a centrally mediated dose-related decrease in blood pressure (BP) and heart rate (HR). Selective perfusion studies indicated that the primary site of action for the hypotension was located in the subarachnoid spaces and a secondary site was identified anterior to the midbrain adjacent to the ventricular spaces. The bradycardia was probably dependent upon an activation of central vagal nuclei and was absent in vagotomized animals. Reflexogenic bradycardia elicited by intravenous norepinephrine or AII was reduced. Similarly, reflex hypotension and bradycardia induced by carotid sinus nerve stimulation were diminished. Tolazoline, IVT, did not produce cardiovascular alterations. However, phenoxybenzamine, IVT, significantly increased BP and HR. d- or 1-propranolol (10 ug/min for 30 min), IVT, did not alter the central hypertensive activity of All. Both isomers significantly reduced BP to an equal extent suggesting that beta-blockade is not necessary for the hypotension. 1-Propranolol, IVT, produced greater reductions in HR which may have been related to the development of peripheral beta-blockade as evidenced by antagonism of intravenous isoproterenol responses.