The authors evaluated the systemic and cerebral hemodynamic and metabolic effects of 1 h of hypotension to a mean arterial pressure of either 50 mmHg or 40 mmHg induced by intravenous adenosine or ATP in dogs maintained on 70% nitrous oxide and 0.1% halothane. Following the hypotensive period, brain biopsy specimens were taken for the determination of cerebral metabolites and calculation of the energy charge. Hypotension induced by either adenosine or ATP produced a marked 40–62% decrease in systemic vascular resistance with little change in cardiac index or oxygen consumption but resulted in a mild metabolic acidosis. Because of a profound decrease in cerebral perfusion pressure with hypotension (to 31–33 mmHg at an MAP of 50 mmHg and 22–24 mmHg at an MAP of 40 mmHg) CBF decreased 54–65% and was inadequate to meet the unchanged cerebral oxygen demands, resulting in some anaerobic metabolism with an accumulation of lactate. While the ease with which one can induce and maintain hypotension with these agents may be advantageous in clinical practice, the effects of adenosine and ATP on cerebral hemodynamics and metabolism may offer no advantage over other hypotensive agents.