The vasomotor responses of individual cerebral pial arterioles on the convexity of the cerebral cortex to subarachnoid perivascular microinjections of dopamine and the putative dopamine receptor agonists, apomorphine, SKF 38393 [2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine] and LY 141865 [trans(+)-4,4a,5,6,7,8,8a,9-octa-hydro-5-propyl-2H-pyrazolo[3,4-g]quinoline hydrochloride], were examined in 38 anesthetized cats. The perivascular microapplication of dopamine (10-9-10-3 M) effected dose-dependent reductions in pial arteriolar caliber, with the maximum reductions in caliber (22 .+-. 2% from preinjection levels: mean .+-. SE) being observed at 10-3 M. The cerebrovascular constriction produced by dopamine (10-5 M) could be significantly attenuated by the concomitant perivascular administration of phentolamine (10-6 M) or methysergide (10-6 M). The perivascular microapplication of apomorphine (10-8-10-4 M) effected dose-dependent increases in arteriolar caliber, with the maximum increase (31 .+-. 6%) being observed with apomorphine (10-5 M). The perivascular administration of the putative dopamine D1-receptor agonist, SKF 38393 (10-9-10-4 M) increased arteriolar caliber with the maximum response (24 .+-. 3%) being observed with injection of 10-7 M. The putative dopamine D2-receptor agonist, LY 141865, also increased cerebral arteriolar caliber, but only at high concentrations (maximum caliber increase 25 .+-. 6.1 with 10-4 M). The cerebrovascular dilatations elicited by apomorphine and by SKF 38393 were markedly attenuated by the concomitant perivascular microapplication of the putative dopamine D1-receptor antagonist, SCH 23390 [R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7-ol] (10-8 M). The perivascular administration of SCH 23390 (10-9-10-5 M) per se did not alter arteriolar caliber nor the arteriolar dilatation provoked by microinjections of acidic CSF. Dopamine receptors (probably of D1 subtype) mediating dilatation may be present on cat cerebral arterioles.