Key result
Ethanol reduced the amplitude of spontaneous and ACh-induced duodenal contractions in vitro, an effect antagonized by charybdotoxin, suggesting involvement of Ca2+-activated K+ channels.
Ca2+-activated K+ channels appear to mediate ethanol-induced duodenal dysmotility in vitro.
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Hypothesis-generating for K+ channel mediation of ethanol effects on gut motility; leaves open in vivo relevance and clinical translation.
The purpose of this study was to investigate the role of K+ channels in duodenal dismotility induced by ethanol in vitro. The amplitude of spontaneous contractions was reduced by ethanol in longitudinal and circular muscle, while frequency did not change. Charybdotoxin antagonized ethanol-induced inhibition of the amplitude of spontaneous contractions. Ethanol decreased ACh-induced contractions and this effect was cancelled out by charybdotoxin. Ca2+-activated K+ channels may be involved in duodenal dismotility induced by ethanol.
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Fagundes et al. (2007) studied Duodenal dysmotility. Ethanol and Charybdotoxin was evaluated on Amplitude of spontaneous and ACh-induced contractions. Ethanol reduced the amplitude of spontaneous and ACh-induced duodenal contractions in vitro, an effect antagonized by charybdotoxin, suggesting involvement of Ca2+-activated K+ channels.
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