Nitric oxide regulates migrating motor complex cycling and its postprandial disruption

¹ Departments of Surgery and Physiology and Digestive Disease Research Center, Medical College of Wisconsin and Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin 53295

We investigated the role of nitric oxide (NO) in the regulation of migrating motor complex (MMC) cycling during the fasting state and its postprandial disruption. Intravenous infusion of N-nitro-l-arginine methyl ester (l-NAME) first produced a premature MMC and then disrupted MMC cycling for the rest of the day. The cycle length of the MMCs was significantly shorter than the control on the 2nd, 3rd, and 4th day after l-NAME infusion. The gastric cyclic motor activity (CMA) did not usually exhibit a premature cycle on the day of l-NAME infusion but was disrupted by l-NAME infusion; the duration of CMA disruption in the stomach was significantly longer than that of MMC disruption in the small intestine. Infusion of N-nitro-l-arginine (l-NNA) exhibited similar effects. The intravenous infusion of l-NAME also significantly shortened the duration of MMC disruption by a meal. l-Arginine alone had no significant effect on gastrointestinal motor activity during the fasting or the fed state, but when infused with l-NAME, it blocked the effects of NO synthase inhibition. Angiotensin II increased the mean arterial pressure to a level similar to that produced by l-NAME but had no significant effect on the fasting or the fed pattern of gastrointestinal motor activity. We conclude that NO containing nonadrenergic noncholinergic (NANC) neurons play a significant role in regulating MMC and CMA cycling during the fasting state and their disruption by a meal. However, NO may not be the only NANC neurotransmitter to inhibit contractions in the gut; phase I activity in the small intestine persisted during NO synthase inhibition by l-NAME or l-NNA.

nonadrenergic noncholinergic neurons; cyclic motor activity: N-nitro-l-arginine methyl ester; N-nitro-l-arginine; vasoactive intestinal peptide; cholecystokinin

Submitted on November 30, 1992
Accepted on June 3, 1993