The authors had observed that on intraoperative discontinuation of sodium nitroprusside being administered to induce hypotension, mean arterial pressure increased to above the pre-hypotension level. Twelve patients who received hypotensive anesthesia for surgical correction of cerebral aneurysms were studied to evaluate the role of the renin–angiotensin system in this phenomenon. In the awake state, mean arterial pressure was 100 ± 2 torr and plasma renin activity 3.0 ± 0.1 ng/ml/hr. Thirty minutes after the establishment of stable halothane–nitrous oxide anesthesia, mean arterial pressure decreased to 85 ± 1 torr and plasma renin activity increased to 4.4 ± 0.1 ng/ml/hr. No appreciable change in either occurred over the next two hours of operation. During sodium nitroprusside-induced hypotension, mean arterial pressure decreased to 49 ± 2 torr and plasma renin activity increased to 15.2 ± 0.2 ng/ml/hr. Thirty minutes after discontinuation of sodium nitroprusside administration, mean arterial pressure increased to 112 ± 2 torr, which was not only higher than the prehypotension level, but also significantly higher than that recorded in the awake state. Plasma renin activity at that time was 10.9 ± 0.1 ng/ml/hr. As the half-life of plasma renin is 15 min, the data suggest that the persistently increased plasma renin activity is probably responsible for the increase of arterial pressure following sodium nitroprusside-induced hypotension.