“…It is unlikely that prejunctional inhibition of noradrenaline release plays any role in the cerebrovascular vasodilatation observed in the present study, as there is no evidence that the resting tone of pial arterioles in the present conditions has any sympathetic component (see also the lack pf efficacy of phentolamine in the present study in altering arteriolar calibre) (Kuschinsky & Wahl, 1975). A second population of dopamine receptors is present in vascular smooth muscle in a number of vascular beds (for example, renal, coronary, femoral, mesenteric and splenic arteries), and after blockade of the contractile receptor mechanisms (most commonly with phenoxybenzamine) the actions of dopamine and dopamine receptor agonists cause relaxation of these peripheral arteries (Goldberg & Toda, 1975;Goldberg et al, 1978;Hilditch & Drew, 1981;Toda, 1983). The cerebrovascular dilatation mediated via dopamine receptor activation, noted in the present in situ study and in previous in vitro studies (Toda, 1976;Edvinsson et al, 1978;Oudart et al, 1981;Forster et al, 1983), are comparable, at least in general terms, with these peripheral dopamine receptors mediating vascular smooth muscle relaxation.…”