The effects of sodium nitroprusside (SNP) on total, ipsilateral cerebral blood flow (CBF) in the unanesthetized and anesthetized goat was evaluated under four conditions: 1) bolus injection of SNP into the cerebral circulation via the temporal artery; 2) continuous infusion of SNP into the temporal artery in amounts too small to affect the peripheral circulation (0.57–1.14 µg/kg/min); 3) intravenous infusion of SNP; 4) continuous intravenous infusion of SNP with a bolus injection of angiotensin. Small doses (20, 40, and 80 µg) of SNP injected directly in the cerebral circulation of the awake goat produced immediate increases of 21 ± 8, 36 ± 8, and 48 ± 10 per cent, respectively, in CBF lasting 1 to 3 min without causing peripheral cardiovascular changes. The effects of SNP were attenuated by 1.5 per cent halothane anesthesia. Continuous infusion of SNP into the temporal artery in amounts too small to cause peripheral cardiovascular effects produced sustained increases in CBF averaging 31 ± 8 per cent; CBF returned to preinfusion values upon cessation of infusion. Intravenous infusion of SNP in both anesthetized and unanesthetized animals in recommended clinical dosages (3–8 µg/kg/min) produced hypotension but did not significantly alter CBF. However, upon injection of angiotensin (1.43 µg/kg), both peripheral blood pressure and CBF increased sharply, suggesting that SNP may impair autoregulation of CBF. The results of this study indicate that SNP dilates the cerebral vascular system in a way that is probably similar to its effects on other vascular beds.