EVIDENCE FOR DOPAMINERGIC VASODILATOR INNERVATION OF THE CANINE PAW PAD

In chloralose‐anaesthetized dogs pretreated with guanethidine and pancuronium, electrical stimulation (0.2 to 5 Hz) of the peripheral end of the cut tibial nerve caused a frequency‐dependent increase in femoral blood flow which was restricted to the paw pads. This neurogenic vasodilatation was not attenuated by atropine, mepyramine plus burimamide, indomethacin or propranolol. It was, however, attenuated in a dose‐dependent manner by intra‐arterial administration of the dopamine receptor antagonist, ergometrine (0.05 to 0.5 mg). The effect of ergometrine could not be explained by non‐specific effects on axonal conduction or transmission or by vasospasm of the blood vessels of the paw‐pads. In dogs with intact tibial nerves, a pharmacologically similar dilator response localized to the paw‐pads could be elicited by electrical stimulation of loci in the ipsilateral diencephalon and midbrain. This response was not due to inhibition of adrenergic vasomotor tone and was abolished by systemic ganglion blockade or by tibial nerve section as well as by femoral arterial administration of ergometrine. It is suggested that the vasculature of the canine paw pads is innervated by a population of autonomic axons which utilize dopamine or a related substance as a transmitter substance and activation of which causes vasodilation. 1979 British Pharmacological Society