Nitric oxide inhibits the myoelectric activity of the small intestine in dogs.

Intestinal motility in fasted animals shows cyclic changes (MMC) that are interrupted by feeding. The aim of this study was to determine the possible implication of nitric oxide (NO) (that was proposed as nonadrenergic noncholinergic neurotransmitter) in the motor components of MMC in 5 conscious dogs equipped with monopolar electrodes implanted along the small bowel. In fasted dogs with typical MMCs, L-NNA (an inhibitor of NO synthase) (5 mg/kg-h i.v.) decreased the MMC interval from control 80 +/- 7 to 60 +/- 4 min and increased significantly the spike activity. Infusion of L-arginine (L-Arg) (a substrate of NO synthase) (10 mg/kg-h i.v.) increased the MMC interval from control 79 +/- 7 to 96 +/- 8 min and reduced the slow waves with spikes by about 25%. Similar but transient effects were observed when glycerin trinitrate (GTN) (a donor of NO) (1 mg/kg-h) was administered. After ingestion of meal, the MMC cycles were replaced by irregular spike activity with an average of about 35% slow waves with spikes. Infusion of L-Arg (10 mg/kg-h) reduced by about 90% the postprandial spike activity. Also, infusion of GTN (1 mg/kg-h) strongly reduced the postprandial spike activity. L-NNA in fed dogs caused an initial increase in spike activity followed by phase III-like activity. Similar effects were obtained when L-NNA was infused in dogs with fed-like motility patterns induced by i.v. infusion of caerulein (75 pmol/kg-h). L-NNA added to L-Arg infusion reversed in part the changes of intestinal motility patterns induced by L-Arg. We conclude that NO system exerts a tonic inhibitory influence on intestinal myoelectric activity by reducing the frequency of MMC pacesetter and by suppressing the postprandial spike activity.