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Nitric oxide regulates migrating motor complex cycling and its postprandial disruption
S K Sarna1, M F Otterson, R P Ryan
1Department of Surgery, Medical College of Wisconsin, Milwaukee.
Abstract:
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 omega-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 omega-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.
Insights
Nitric oxide (NO) plays a key role in regulating gut motility, specifically the migrating motor complex (MMC) and gastric cyclic motor activity (CMA). NO synthase inhibition disrupts normal gut cycling, affecting fasting and post-meal activity.
Area of Science:
- Gastroenterology
- Neurogastroenterology
- Physiology
Background:
- The migrating motor complex (MMC) is crucial for interdigestive gastrointestinal motility.
- Nonadrenergic noncholinergic (NANC) neurons are implicated in regulating gut functions.
- The precise role of nitric oxide (NO) in MMC cycling and its response to feeding requires further elucidation.
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in regulating the cycling of the migrating motor complex (MMC) during fasting.
- To examine how NO influences the disruption of MMC and gastric cyclic motor activity (CMA) after a meal.
- To identify the specific neurotransmitters involved in NO-mediated gut motility regulation.
Main Methods:
- Intravenous infusion of NO synthase inhibitors, N omega-nitro-L-arginine methyl ester (L-NAME) and N omega-nitro-L-arginine (L-NNA).
- Administration of L-Arginine to assess its effect on NO synthase inhibition.
- Monitoring of gastrointestinal motor activity during fasting and fed states.
- Measurement of mean arterial pressure changes.
Main Results:
- L-NAME infusion induced premature MMC and disrupted MMC cycling, with shorter cycle lengths observed on subsequent days.
- Gastric CMA disruption by L-NAME was longer than MMC disruption in the small intestine.
- L-NAME significantly shortened the duration of meal-induced MMC disruption; L-Arginine blocked these effects.
- Angiotensin II affected blood pressure but not gastrointestinal motor activity.
Conclusions:
- Nitric oxide (NO)-containing nonadrenergic noncholinergic (NANC) neurons are significant regulators of MMC and CMA cycling during fasting and postprandial states.
- NO plays a crucial role in the disruption of gut motility patterns by meals.
- While NO is important, other NANC neurotransmitters may also contribute to inhibiting gut contractions, as evidenced by persistent phase I activity during NO synthase inhibition.