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Guanethidine abolished the inhibitory response of segments of rabbit intestine to stimulation of the sympathetic nerves which accompany the mesenteric arteries. In the majority of experiments a motor response of the intestinal segment was then revealed; it was more readily observed in intestinal segments from young than from adult rabbits. The motor response of the intestine to sympathetic stimulation after guanethidine was blocked by atropine. It was not blocked by hexamethonium and was present in rabbits in which the vagal innervation to the small intestine had been sectioned. In the cat isolated atria, guanethidine blocked the accelerator response to sympathetic nerve stimulation and revealed a response resembling that to stimulation of the vagus. It was concluded that guanethidine blocked the release of noradrenaline and thus revealed the response to the direct action of acetylcholine released from cholinergic sympathetic nerves.

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.

It has been shown by others that hemicholinium (alpha,alpha'-dimethylethanolamino-4,4'-biacetophenone) inhibits the synthesis of acetylcholine, an effect which is reversed by choline. Hemicholinium produces a failure of response to nerve stimulation in the following sympathetically innervated preparations: guinea-pig isolated vas deferens, rabbit isolated uterus, rabbit isolated colon, perfused rabbit ear, cat isolated atria and the piloerector muscles in the cat's tail. The blocking action of hemicholinium on the responses to postganglionic sympathetic stimulation resembles its blocking action against cholinergic nerve stimulation observed on rabbit isolated atria with vagus nerves, rabbit isolated vagina with pelvic nerves, and guinea-pig isolated diaphragm with phrenic nerve. The failure of transmission produced by hemicholinium in sympathetic nerves and in cholinergic nerves can be reversed by choline. It is suggested that if there were a cholinergic junction at sympathetic nerve endings the mechanism of the blocking action of hemicholinium at these endings could be explained by inhibition of acetylcholine synthesis.

Direct evidence is given that reserpine, in concentrations of 0.125 to 0.625 mM, effects a release of noradrenaline from a suspension of transmitter granules isolated from bovine splenic nerves.