Femoral vasodilatation produced by piribedil (ET495) and its metabolite S584 in the hindleg of the dog.

On local injection into the innervated hindleg of the dog piribedil, like apomorphine, produced a vasodilatation blocked by haloperidol. S584, the catechol metabolite of piribedil, produced a vasodilatation which was not blocked by haloperidol. Neither propranolol nor atropine influenced the vasodilatation produced by piribedil or S584. Denervation of the hindleg abolished the responses to piribedil and S584. During the infusion of noradrenaline into the denervated hindleg, the responses to S584 reappeared but those to piribedil did not. It is concluded from these experiments that the vasodilatation produced by piribedil in the innervated hindleg of the dog, like that of apomorphine, is mediated by dopamine receptors and that the effect of piribedil cannot be explained by the formation of its catechol metabolite S584.