Role of nitric oxide in esophageal peristalsis

In vitro studies have suggested that NO may be a nonadrenergic, noncholinergic inhibitory mediator in the esophageal body. We examined the role of NO in physiological peristalsis in anesthetized opossums by assessing the effect of the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) on esophageal contractions induced by swallows, prolonged vagal efferent nerve stimulation, and midesophageal balloon distension. A perfused manometry system measured intraluminal pressures 1 and 5 cm orad to the lower esophagus, and suction electrodes monitored membrane potential changes at the same locations. NO synthase inhibition 1) decreased swallow-induced contraction amplitude in the distal esophagus and, when combined with atropine, abolished these contractions; 2) diminished swallow-induced contraction latencies, predominantly in the distal esophagus, thereby decreasing the latency gradient and increasing the peristaltic velocity; 3) abolished vagal-stimulation-induced, end-of-stimulus "B" contractions and either unmasked or increased the amplitude of intrastimulus "A" contractions; 4) abolished the contractions occurring at the end of balloon distension; and 5) inhibited the membrane hyperpolarization and the subsequent nonadrenergic, noncholinergic depolarization induced by all three stimuli. These data support the hypothesis that NO is a mediator of nonadrenergic, noncholinergic neurotransmission in the opossum esophagus. Furthermore, the data suggest that esophageal peristalsis is mediated by a "blended" activation of cholinergic and nonadrenergic, noncholinergic (via NO) neurons.