The cardiovascular actions of N,N-Di-n-propyldopamine (DPDA), a dopamine receptor agonist, and the directly acting vasodilator sodium nitroprusside have been compared in both conscious and chloralose-anaesthetised dogs. Bolus intravenous doses of DPDA (6.5-32 micrograms/kg) and sodium nitroprusside (3-10 micrograms/kg) induced dose-related falls in blood pressure associated with reflex tachycardia in both preparations. The dopamine receptor antagonist sulpiride (0.5 mg/kg) eliminated these effects of DPDA and its ability to reduce renal and femoral vascular resistances in the chloralose-anaesthetised dog, but did not influence the actions of sodium nitroprusside. Ganglion blockade (hexamethonium, 5-10 mg/kg alone or in a combination with atropine, 1 mg/kg) abolished the reflex tachycardia to both compounds and potentiated the depressor effects of sodium nitroprusside but either reduced or did not alter the hypotension produced by DPDA. The renal dilator response to DPDA was also reduced, while femoral vasodilation was abolished. This study illustrates that DPDA can reduce blood pressure in conscious and chloralose-anaesthetised dogs but that this effect is accompanied by reflex tachycardia. Inhibitory dopamine receptors on sympathetic nerves, and to a lesser extent postjunctional (vascular) dopamine receptors, are involved in these actions of DPDA.