Background & Aims: 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 . Methods: 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. Results: In the LES, atropine inhibited tonic contractions, whereas N^ω-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. Conclusions: 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.

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The actions of caffeine and ryanodine on the spontaneous rhythmic activities in the guinea-pig colon were studied by mechanical tension recording. Caffeine reduced the amplitude of the spontaneous rhythmic activity at low concentration (0.3 mM-1 mM). At high concentration (3-10 mM), it induced a phasic transient contraction. The spontaneous rhythmic activity and a phasic contraction induced by caffeine, were blocked by verapamil (3μM) or by removal of external Ca²⁺.Ryanodine affected neither resting tension nor frequency of spontaneous activity at 1μM. However in the circular muscle strips pretreated with ryanodine, a sustained contraction was initiated after the removal of caffeine (10mM).Continuous Ca²⁺ influx was necessary for spontaneous rhythmic activities and a phasic transient contraction, because it was abolished completely by the removal of external Ca2+. Verapamil (3μM), a voltage gated L-type Ca²⁺channels blocker, inhibited the spontaneous rhythmic activities and also inhibited phasic transit contraction followed by a sustained contraction induced by 10 mM caffeine. Our results suggest that caffeine may produce a sustained contraction by activating verapamil sensitive Ca²⁺ channel. In the muscle pretreated with both caffeine and ryanodine, continuous Ca²⁺ influx may occur alsothrough verapamil sensitive pathway.

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