Abstract

Apomorphine, injected into the dog femoral artery in doses of 0.6 microng or higher, produced a marked increase in femoral blood flow, without a change in blood pressure. No increase in flow was produced by comparable doses of dopamine or morphine. After sympathetic denervation or administration of phenoxybenzamine, the apomorphine vasodilatation was either abolished or greatly reduced. When the vascular tone in the denervated hindleg was restored by sympathetic nerve stimulation, the vasodilatory effect of apomorphine often re-established itself; this was not the cases when the vascular tone was restored by an infusion of noradrenaline. The apomorphine vasodilatation was not antagonized by propranolol or atropine. Mepyramine, in doses that antagonize histamine, often inhibited the apomorphine vasodilatation. Haloperidol, injected i.a., antagonized the apomorphine effect without changing the responses to isopropylnoradrenaline, acetylcholine, histamine and and nitroglycerin. Haloperidol blockade was overcome by increasing the dose of apomorphine. These results suggest that apomorphine dilates the femoral vasculature by an action on a "dopamine receptor." The possibility that the receptor is located on sympathetic nerve endings is discussed.