Mechanism of the noradrenergic motor control on the lower oesophageal sphincter in the cat.

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Abstract
The release of labeled acetylcholine was measured on lower esophageal sphincter (l.o.s.) muscular strips previously loaded with tritiated choline. This release was greatly increased by noradrenaline [norepinephrine] 10-5 g/ml and unaffected by atropine 10-6 g/ml, but it was practically abolished if hemicholinium 5.2 .times. 10-4 M was added to the incubating bath containing the tritiated choline. An autoradiographic study of sections of l.o.s. strips loaded with tritiated choline showed that the radioactivity was mainly located in the nerve cells of the enteric plexuses and that the muscle cells were very poorly labeled. The increased release of acetylcholine induced by noradrenaline did not occur in a Ca2+-free or in a hypermagnesic Tyrode (12 mM). Tetrodotoxin 10-6 g/ml had no effect on the increased release of acetylcholine induced by noradrenaline. Sucrose gap recordings showed that the depolarizing effect of noradrenaline on l.o.s. muscular strips was unaffected by tetrodotoxin 10-6 g/ml. Acetylcholine released in the l.o.s. under the action of noradrenaline apparently originated from the synaptic endings of the cholinergic intramural neurons.