Consistent unmasking of dopamine-induced dilation of the canine femoral vascular bed.

Dopamine (DA) produced dose-related vasodilation in the canine femoral vascular bed after the administration of two alpha adrenergic blocking agents, WR-149,024 (1,18-diamino-6,13-diaza-9,10-dithiaoctadecane) or yohimbine. DA-induced vasodilation unmasked by yohimbine was not antagonized by propranolol, pyrilamine and metiamide, hexamethonium or atropine, but was attenuated selectively by the DA antagonist, sulpiride. The R-enantiomer of sulpiride was more effective than the S-enantiomer in attenuating DA-induced dilation. Phenoxybenzamine produced moderate (apparently nonspecific) attenuation of vasodilator responses to DA. The weaker vascular DA agonist, N,N-di-n-propyl dopamine, was approximately 1/25 as potent as DA in eliciting femoral vasodilation after yohimbine treatment. These findings suggest that DA produces femoral vasodilation after WR-149,024 or yohimbine by activation of vascular DA receptors similar to those proposed to exist in the renal vascular bed.