Intraventricular infusion of angiotensin II (50, 100, and 200 ng/kg per min) produced significant elevations of arterial blood pressure (20-25%) in alpha-chloralose-anesthetized cats. The pressor responses were not accompanied by significant changes in heart rate,cardiac output, or contractility and were chiefly due to significant increases in total peripheral resistance. In contrast, pressor responses to intravenous infusion of angiotensin II (100 ng/kg per min) were accompanied by reflex decrease in cardiac activity. While intravenous angiotensin II caused increases in the resistance of skeletal, mesenteric, and renal vasculature, the intraventricular administration of angiotensin II increased resistance only in the mesenteric and renal vasculature. Further, centrally administered angiotensin II significantly enhanced urinary output and the rate of Na+ excretion both in the intact as well as in the denervated kidneys. However, the diuretic and natriuretic effects were significantly greater in the intact than in the denervated kidneys, indicating a centrally mediated neurogenic mechanism. The significant increase in the urinary concentration of Na+ (mEq/liter) following intraventricular angiotensin appeared to be secondary to the elevation of arterial blood pressure, since this effect was unaltered by acute renal denervation. The results of this investigation are consistent with the hypothesis that an elevation in the concentration of angiotensin II within the cerebrospinal fluid may trigger neurogenic mechanisms resulting in the constriction of glomerular efferent arterioles. Such an effect would be expected to increase glomerular filtration pressure and filtration fraction, and may play a role in the diuretic and natriuretic effects noted.