Role of nitric oxide in esophageal peristalsis in the opossum.

To explore the involvement of NO in normal peristalsis, the effects of inhibitors of NO synthase, including N omega-nitro-L-arginine (L-NNA) and N omega-nitro-L-arginine methyl ester (L-NAME), on esophageal peristaltic contractions induced by diverse stimuli that may involve different neuronal circuits were studied. Studies were performed in opossums. Experimental conditions in vivo included primary peristalsis (P) induced by pharyngeal stroking, short-train (1 second) electrical stimulation of the vagus nerve which caused peristaltic (S) contractions, and long-train (10 second) electrical stimulation of the vagus nerves which caused contractions at the onset of (A contractions) and after (B contractions) the stimulation period. In vitro experiments were performed on strips of esophageal circular muscle using electrical field stimulation which caused contractions at the onset of (on contractions) and after (off contractions) the stimulation period. The administration of L-NAME significantly decreased the latency period and reduced the latency gradient for P contractions, thereby increasing the velocity of peristalsis. Concomitant administration of atropine prolonged the latency period but did not restore the latency gradient. L-NAME abolished B contractions in a dose-dependent fashion. In vitro, L-NAME caused dose-dependent inhibition of off contractions and augmentation of on contractions. These studies support the hypothesis that NO may be involved in (a) both the latency period and the latency gradient, as well as in the contraction amplitude of esophageal peristalsis; and (b) esophageal B and off contractions.