Calcium-dependence of the adenosine-induced renal vasoconstriction was studied in dogs anaesthetized with pentobarbital. Close intraarterial (i.a.) infusion of adenosine (40 and 100 micrograms X min-1) elicited a significant blood flow decrease followed by partial recovery during the 2 min infusion periods as measured with an electromagnetic flow probe. I.a. infusion of verapamil (100 micrograms X min-1) blocked the constrictor response. Verapamil also reduced the vasoconstriction produced by i.a. angiotensin II (0.1 micrograms X min-1) or adrenaline (0.6 micrograms X min-1). Blood pressure remained unchanged throughout all the interventions. The results indicate that the adenosine-induced renal vascular response depends on the availability of extracellular Ca2+ to the contractile mechanism of smooth muscle, a property shared by other well known renal constrictor agents.