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Am J Physiol Gastrointest Liver Physiol 266: G123-G131, 1994;
0193-1857/94 $5.00
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AJP - Gastrointestinal and Liver Physiology, Vol 266, Issue 1 123-G131, Copyright © 1994 by American Physiological Society


ARTICLES

Role of nitric oxide in esophageal peristalsis

N. Anand and W. G. Paterson
Gastrointestinal Diseases Research Unit, Queen's University, Kingston, Ontario, Canada.

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.


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