THE ANTAGONISM OF COCAINE TO THE ACTION OF CHOLINE 2,6‐XYLYL ETHER BROMIDE AT SYMPATHETIC NERVE ENDINGS

Abstract

Choline 2,6-xylyl ether bromide (TM10) prevents contraction of the nictitating membrane and of the spleen in response to sympathetic nerve stimulation. It was confirmed that this effect was due to prevention of the release of noradrenaline (“sympathin”) at the nerve endings. The intravenous injection of cocaine before choline xylyl ether blocked the action of the latter drug. However, when atropine was injected before the cocaine the effects of large doses of choline xylyl ether were not completely blocked. After block had been produced by choline xylyl ether the injection of cocaine partially restored both the secretion at the sympathetic nerve endings and the responses of the organs supplied by the nerves. Phenoxybenzamine did not restore the secretion at the nerve endings after it had been inhibited by choline xylyl ether, indicating that the latter did not cause an increased uptake of sympathin by the receptors.