Central and regional cardiovascular responses to step changes in carotid sinus pressure were evaluated in dogs before and after increasing carotid sinus reflex set point pressure, by approximately 30%, via an intravenous infusion of angiotensin II at three anesthetic levels (isoflurane). With respect to overall cardiovascular behavior, angiotensin inhibited both the interaction of carotid sinus baroreceptor stimulation and anesthesia upon mean arterial pressure and total resistance, together with the inverse relationship between iliac resistance and carotid sinus pressure. At the set point pressure of the carotid sinus reflex, angiotensin increased set point levels of aortic, celiac, mesenteric and renal resistances, reduced corresponding set point flows, and increased the range of arterial pressure control together with the maximum capacity of the carotid sinus reflex to increase mean aortic pressure and power for all anesthetic levels. Angiotensin increased the set point sensitivity of mean arterial pressure (gain), heart rate, iliac blood flow, aortic, celiac, mesenteric and renal resistance, to changes in carotid sinus pressure for intermediate anesthetic levels. While reflex gain was unchanged by angiotensin, peak gain was significantly increased at lower anesthetic levels. The maximum capacity of the carotid sinus reflex to decrease mean aortic pressure and power was reduced. Thus, intravenous angiotensin infusion producing moderate increases in mean arterial pressure facilitates the ability of the carotid sinus baroreceptors to control mean arterial pressure and heart rate, and results in an increased overall vasoconstrictor capacity. Corresponding increased ability to control regional blood flow was confined to the iliac bed.