Central and splanchnic hemodynamic effects during controlled hypotension induced by the administration of the endogenous vasodilator adenosine were studied in ten artificially ventilated dogs under neurolept anesthesia. Adenosine was administered as a continuous infusion in the aorta (n = 3), in the inferior vena cava (n = 3), and after pretreatment with dipyridamole (which inhibits the cellular uptake of adenosine) (n = 4) in a dose sufficient to maintain a mean arterial blood pressure (MABP) level of approximately 50 mmHg. Observations were made before and after 20 min of controlled hypotension. Basal arterial plasma levels of adenosine were in the 10−7M range (&OV0398; = 0.4 μM). The hemodynamic response was similar in all three settings. Adenosine caused a profound decrease in systemic vascular resistance (SVR) (52%,P< 0.01) and preportal vascular resistance (PPR) (64%,P< 0.01), while hepatic arterial vascular resistance (HAR) increased by 49% (P< 0.05). Cardiac output increased (22%,P< 0.05) through increase of stroke volume (77%,P< 0.01), while heart rate decreased (28%,P< 0.01). Whole-body oxygen uptake decreased (14%,P< 0.01). Portal venous blood flow increased by 28% (P< 0.05), whereas hepatic arterial blood flow decreased by 70% (P< 0.01). In the preportal tissues, oxygen uptake decreased by 21% (P< 0.01). In contrast, hepatic oxygen consumption increased (53%,P< 0.05). Adenosine-induced hypotension was not associated with changes in plasma renin activity or the plasma concentration of norepinephrine. It is concluded that adenosine causes a rapidly induced and easily maintained hypotension and may be a potentially useful agent for controlled hypotension in patients.