Abstract
ObjectiveAcute administration of 5-hydroxytryptamine4 (5-HT4) receptor agonist, mosapride or esophageal infusion of the transient receptor potential vanilloid receptor-1 (TRPV1) agonist capsaicin promotes secondary peristalsis. We aimed to investigate whether acute esophageal instillation of capsaicin-containing red pepper sauce or administration of mosapride has different effects on the physiological characteristics of secondary peristalsis.MethodsSecondary peristalsis was induced with mid-esophageal air injections in 14 healthy subjects. We compared the effects on secondary peristalsis subsequent to capsaicin-containing red pepper sauce (pure capsaicin, 0.84 mg) or 40 mg oral mosapride.ResultsThe threshold volume for generating secondary peristalsis during slow air distensions was significantly decreased with capsaicin infusion compared to mosapride (11.6 ± 1.0 vs. 14.1 ± 0.8 mL, P = 0.02). The threshold volume required to produce secondary peristalsis during rapid air distension was also significantly decreased with capsaicin infusion (4.6 ± 0.5 vs. 5.2 ± 0.6 mL, P = 0.02). Secondary peristalsis was noted more frequently in response to rapid air distension after capsaicin infusion than mosapride (80% [60–100%] vs. 65% [5–100%], P = 0.04). Infusion of capsaicin or mosapride administration didn’t change any parameters of primary or secondary peristalsis.ConclusionsEsophageal infusion with capsaicin-containing red pepper sauce suspension does create greater mechanosensitivity as measured by secondary peristalsis than 5-HT4 receptor agonist mosapride. Capsaicin-sensitive afferents appear to be more involved in the sensory modulation of distension-induced secondary peristalsis.
Highlights
Primary peristalsis is initiated by a swallow and is the main source of esophageal transit whereas distension-induced or secondary peristalsis functions to maintain an empty esophagus by clearing refluxate from the stomach [1] in the absence of swallowing
Capsaicin-sensitive afferents appear to be more involved in the sensory modulation of distension-induced secondary peristalsis
The control of secondary peristalsis in the striated muscle is modulated by central mechanisms with vagal afferents, which subsequently results in sequential vagal efferent discharge to the striated musculature of the proximal esophagus [7], while secondary peristalsis in the smooth muscle part is controlled by an intrinsic neuromuscular reflex
Summary
Primary peristalsis is initiated by a swallow and is the main source of esophageal transit whereas distension-induced or secondary peristalsis functions to maintain an empty esophagus by clearing refluxate from the stomach [1] in the absence of swallowing. Distension-induced secondary peristalsis has been extensively studied regarding its physiological characteristics and clinical applications in a variety of esophageal symptoms and disorders such as nonobstructive dysphagia and gastroesophageal reflux disease (GERD) [2,3,4,5,6]. The intrinsic reflex that modulates secondary peristalsis includes mucosal and intramuscular mechanoreceptors which contribute to initiate and propagate peristalsis [8, 9]. Previous studies have demonstrated that secondary peristaltic activity and distension sensitivity can be enhanced by esophageal infusion with capsaicin-containing red pepper sauce [14]. Subsequent work has shown that continued exposure of the esophagus to capsaicin infusion is characterized by the activation of TRPV1 receptors and desensitization of secondary peristalsis [15]
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