Electric and motor effects of autonomic drugs on longitudinal esophageal smooth muscle

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Abstract
Strips from the lowest 2 cm of cat esophagus were mounted in a bath to record tension and electrical activity in the longitudinal muscle at rest and in response to autonomic drugs. At rest there were few or no contractions. Electrical slow waves occurred rarely. Bursts of spike potentials accompanied slow waves during contractions. There were no qualitative differences between spontaneous electrical events and those produced by drugs. Cholinergic drugs always caused contractions. Epinephrine and nor-epinephrine caused contractions opposed by tolazoline. Isopropyl-norepinephrine was inhibitory and was opposed by propranolol. Excitation from norepinephrine was antagonized by atropine and hemicholinium. Anoxia reduced the response to norepinephrine. The norepinephrine effect was sometimes reduced by removing tissue overlying the muscle. Sensitivity to norepinephrine varied widely. The response to norepinephrine could be potentiated by physostigmine. Nicotine and hexame-thonium did not affect the response to norepinephrine. The results indicate that adrenergic a-receptors are excitatory, and [beta]-receptors, inhibitory. [alpha]-Receptors appear to be located in postganglionic cholinergic nerves present, in part, in the esophageal plexus. [beta]-Receptors lie in the smooth-muscle cells.