Dopamine produces dilation predominantly in renal and mesenteric vascular beds. An action on a specific receptor has been confirmed in vitro using a perfused canine mesenteric vessel preparation. Reductions in resistance produced by dopamine are selectively inhibited by methylergometrine (pA2 = 8.3) and sulpiride (pA2 = 5.6). Evidence is accumulating which suggests that vascular dopamine receptors are innervated. Periaterial nerve stimulation in anesthetized dogs produces increases in blood flow in the superior mesenteric artery which are not influenced by atropine and propranolol but are inhibited by haloperidol. Dopamine receptors are also present at sympathetic ganglia and sympathetic nerve terminals. Inhibition of noradrenaline release resulting from stimulation of these receptors may make an important contribution to the depressor effects of dopamine receptor agonists in anesthetized animals and in man. Reductions in blood pressure induced by bromocriptine and other long-acting dopamine receptor stimulants are frequently associated with reductions in heart rate, but not always with a corresponding depression of myocardial contractile force. This phenomenon may be explained by a selective distribution of prejunctional receptors in sympathetic neurons innervating the sinus node.