N,N-di-n-propyl dopamine (DPDA) dilates the renal vascular bed by action on dopamine (DA) vascular receptors. In phenoxybenzamine-treated dogs DPDA caused dose-related increments in renal blood flow with an ED50 approximately 15 to 30 times greater than DA. The renal vasodilation was not antagonized by propranolol, antihistamines, atropine or hexamethonium, but was attenuated specifically by the DA antagonists metoclopramide and haloperidol. DPDA lacked beta adrenergic activity. In doses up to 480 microgram/kg i.v. DPDA had no effect on cardiac contractile force, whereas the minimal effective dose of DA is usually less than 8 microgram/kg. Increments in femoral or renal blood flow produced by DPDA were not antagonized by propranolol. DPDA and DA also differed in their effects on the femoral vascular bed. Before administration of phenoxybenzamine DPDA caused vasodilation while DA typically produced dose-related vasoconstriction. DPDA-induced femoral vasodilation was markedly attenuated by phenoxybenzamine and hexamethonium in contrast to renal vasodilation which was not affected by these drugs. DPDA was also a weaker vasoconstrictor than DA. These findings demonstrate that it is possible to synthesize DA vascular agonists with qualitatively different pharmacological profile than DA.