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The aim of the present study was to clarify roles of ATP-dependent potassium channels (K ATP channels) in motility of the striated muscle portion in the esophagus. An isolated segment of the rat esophagus was placed in an organ bath and mechanical responses were recorded using a force transducer. Electrical stimulation of the vagus nerve evoked contractile response of striated muscle in the esophageal segment. Application of glibenclamide, an antagonist of K ATP channels, increased amplitude of vagally mediated twitch contractions of the rat esophagus. On the other hand, minoxidil, an agonist of K ATP channels, decreased amplitude of twitch contractions. RT-PCR revealed the expression of subunits of K ATP channels in esophageal tissue. In addition, immunopositivity for subunits of K ATP channels was observed in the striated muscle cells of the esophageal muscle layer. These findings indicate that K ATP channels contribute to motor regulation of striated muscle in the rat esophagus.

Background: Esophageal peristalsis is controlled by the brainstem via vago-vagal reflex. However, the precise regulatory mechanisms in the striated muscle portion are largely unknown. The aim of this study was to characterize peristaltic motility in the portion of the esophagus using a novel in vivo method in rats., Methods: A balloon-tipped catheter was placed in the esophagus of a rat anesthetized with urethane. To induce esophageal peristalsis, the balloon was inflated by water injection., Key Results: When the balloon was inflated near the bronchial bifurcation, the balloon was transported in the aboral direction. Vagotomy abolished the peristaltic response. The threshold volume for inducing esophageal peristalsis varied according to the velocity of balloon distention; the volume being effective to induce peristalsis at a low inflation speed was smaller than the threshold volume at a rapid inflation speed. Even in the absence of inflation, keeping the balloon inside the esophagus during an interval period prevented subsequent induction of peristaltic motility. In addition, a nitric oxide synthase inhibitor abolished the induction of esophageal peristalsis., Conclusions and Inferences: Our findings suggest that (a) in addition to the intensity, the velocity of distention is important for activating the mechanosensory mechanism to induce esophageal peristalsis, (b) tonic inputs from afferent fibers located at the mucosa may reduce the excitability of mechanosensors which is necessary for inducing peristalsis, and (c) nitric oxide plays essential roles in the induction of esophageal peristalsis. These results provide novel insights into the regulatory mechanisms of esophageal motility., (© 2018 John Wiley & Sons Ltd.)

Background Serotonin (5-hydroxytryptamine, 5- HT) is a regulatory factor in motility of the gastrointestinal tract including the esophagus. Although we proposed that vagal cholinergic and mast cell-derived non-cholinergic components including serotonin coordinately shorten the esophagus, the precise mechanism of serotonin-induced contractions in the suncus esophagus is still unclear. Therefore, the aims of this study were to determine characteristics of contractile responses induced by serotonin and to identify 5- HT receptor subtypes responsible for regulating motility in the suncus esophagus. Methods An isolated segment of the suncus esophagus was placed in an organ bath, and longitudinal or circular mechanical responses were recorded using a force transducer. Key Results Serotonin evoked contractile responses of the suncus esophagus in the longitudinal direction but not in the circular direction. Tetrodotoxin did not affect the serotonin-induced contractions. Pretreatment with a non-selective 5- HT receptor antagonist or double application of 5- HT1 and 5- HT2 receptor antagonists blocked the serotonin-induced contractions. 5- HT1 and 5- HT2 receptor agonists, but not a 5- HT3 receptor agonist, evoked contractile responses in the suncus esophagus. Conclusion & Inferences The findings suggest that serotonin induces contractile responses of the longitudinal smooth muscle in the muscularis mucosae of the suncus esophagus that are mediated via 5- HT1 and 5- HT2 receptors on muscle cells. The serotonin-induced contractions might contribute to esophageal peristalsis and emetic response. [ABSTRACT FROM AUTHOR]