We examined whether Ang II receptors in the CNS mediate hemodynamic responses to pharmacological (cocaine) and behavioral (cold water) stressors. Following cocaine (5 mg/kg, iv), rats were classified as vascular responders (VR) if their pressor response was due entirely to an increase in systemic vascular resistance (SVR) and despite a decrease in cardiac output (CO). Cocaine elicited a pressor response in mixed responders (MR) that was dependent on small increases in both SVR and CO. Ang II (30 ng/5 µL icv, 5 min prior to cocaine) augmented the decrease in CO in VR and prevented the increase in CO in MR. Administration of [Sar¹, Thr⁸]-Ang II (20 µg/5 µL icv, sarthran) prior to cocaine attenuated the decrease in CO and the large increase in SVR in VR so that they were no longer different from MR. Losartan (20 µg, icv) or captopril (50 µg, icv) preceding cocaine administration also attenuated the decrease in CO and the large increase in SVR seen in VR only. The role of angiotensin was not specific for cocaine since Ang II (icv) prior to startle with cold water (1 cm deep) enhanced the decrease in CO and increase in SVR in both MR and VR whereas losartan (icv) pretreatment before startle attenuated the decrease in CO and increase in SVR in VR so that they were no longer different than MR. These data suggest that central Ang II receptors mediate the greater vascular and cardiac responsiveness in vascular responders to acute pharmacological and behavioral stressors.