Neuronal control of motility changes in the canine lower esophageal sphincter and stomach in response to meal ingestion.

Abstract

Neuronal control of motility changes in the lower esophageal sphincter (LES), gastric body (GB) and gastric antrum (GA) in response to meal ingestion is not fully understood. The aim of this study was to investigate the neuronal mechanism of the LES and gastric motility response to meal ingestion in conscious dogs. Dogs fitted with force transducers in the LES, GB and GA were given neuronal antagonists before a meal. Motility was assessed for 10 min after feeding and was compared to results without antagonists. In the LES, atropine inhibited tonic contractions, whereas N omega-nitro-L-arginine (L-NAME) significantly enhanced tonic contractions initiated by meal ingestion. In the GB, atropine, hexamethonium or L-NAME inhibited receptive relaxation, and the effect of hexamethonium was significantly greater than that of atropine or L-NAME. In the GA, atropine, hexamethonium or naloxone inhibited postprandial phasic contractions, whereas L-NAME tended to enhance phasic contractions. Neuronal control of postprandial motility was clearly different in each region: (1) LES tonic contractions are mainly regulated by muscarinic receptors, (2) nicotinic transmission plays an essential role in receptive relaxation, which also involves muscarinic receptors and nitric oxide, (3) cholinergic nerves and opiate receptors are involved in the occurrence of antral phasic contractions, and (4) endogenous nitric oxide may inhibit postprandial contractions in the LES and GA.