Abstract
1 The possibility of a vasodilator innervation to the isolated and perfused central artery of the rabbit ear was examined. 2 Stimulation of the periarterial nerves in the presence of noradrenaline or other agonist used to maintain a partial constriction of the ear artery, led to a decrease in intraluminal flow followed after the cessation of stimulation by an increase in flow beyond the pre-stimulation level. 3 After blockade of adrenergic transmission with bretylium or guanethidine or of the α- and β-adrenoceptors with phentolamine and propranolol, stimulation of the periarterial nerves in the presence of a background tone, led to a clearly detectable vasodilatation. This dilatation was not blocked by treatment with atropine or mepyramine; nor was it enhanced by physostigmine. 4 Pretreatment of rabbits with reserpine (2 mg/kg) to deplete catecholamine stores, eliminated both the vasoconstrictor and vasodilator responses to nerve stimulation. However, a lower dose of reserpine (0.2 to 0.5 mg/kg) selectively eliminated the vasoconstrictor component of periarterial nerve activation. 5 The ear artery dilated in response to low concentrations of prostaglandin E1, and E2, in the presence of noradrenaline, but treatment with inhibitors of prostaglandin synthesis, indomethacin, aspirin or eicosa-5,8,11,14-tetraynoic acid did not reduce the vasodilator response. Attempts to extract a prostaglandin in the bathing medium were unsuccessful. 6 The involvement of a purine nucleotide appeared unlikely since the ear artery dilated only in response to fairly high concentrations of adenosine 5′-triphosphate (ATP), adenosine 5′-diphosphate (ADP) and adenosine 5′-monophosphate (AMP). Furthermore, dipyridamole, an inhibitor of adenosine uptake, enhanced dilatation due to exogenous ATP but not to periarterial nerve stimulation. 7 It is concluded that the central artery of the rabbit ear has a vasodilator innervation but the identity of the transmitter remains to be established.