Vasomotor responses of cerebral arterioles in situ to putative dopamine receptor agonists

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Abstract
1 The vasomotor responses of individual cerebral pial arterioles on the convexity of the cerebral cortex to subarachnoid perivascular micro-injections of dopamine and the putative dopamine receptor agonists, apomorphine, SKF 38393 and LY 141865, have been examined in 38 anaesthetized cats. 2 The perivascular microapplication of dopamine (10−9–10−3 M) effected dose-dependent reductions in pial arteriolar calibre, with the maximum reductions in calibre (22 ± 2% from preinjection levels: mean ± s.e.) 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). 3 The perivascular microapplication of apomorphine (10−8–10−4 M) effected dose-dependent increases in arteriolar calibre, with the maximum increase (31 ± 6%) being observed with apomorphine (10−5 M). 4 The perivascular administration of the putative dopamine D1-receptor agonist, SKF 38393 (10−9–10−4 M) increased arteriolar calibre, 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 calibre, but only at high concentrations (maximum calibre increase 25 ± 6.1 with 10−4 M). 5 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 (10−8 M). The perivascular administration of SCH 23390 (10−9–10−5 M) per se did not alter arteriolar calibre nor the arteriolar dilatation provoked by microinjections of acidic cerebrospinal fluid. 6 These results point to the presence on cat cerebral arterioles of dopamine receptors (probably of D1 subtype) mediating dilatation.