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Alcohol and Alcoholism Advance Access originally published online on May 28, 2007
Alcohol and Alcoholism 2007 42(4):291-295; doi:10.1093/alcalc/agm037
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Copyright © The Author 2007. Published by Oxford University Press on behalf of the Medical Council on Alcohol.

Ca2+-activated K+ channels involved in duodenal dismotility induced by ethanol{dagger}

D. S. Fagundes, L. Grasa, M. P. Arruebo, M. A. Plaza and M. D. Murillo*

Departamento de Farmacología y Fisilogía (Fisiología), Facultad de Veterinaria, Universidad de Zaragoza, Miguel Servet 177, 50013 Zaragoza, Spain

* Author to whom correspondence should be addressed at: Departamento de Farmacología y Fisiología (Fisiología), Facultad de Veterinaria, Universidad de Zaragoza, Miguel Servet 177, 50013 Zaragoza Spain. Tel.: 34-976-761652; Fax: 34-976-761612; E-mail: dmurillo{at}unizar.es

Received 24 November 2006; first review notified 27 January 2007; ; accepted 30 March 2007


  Abstract

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.

{dagger} Part of the results were presented at the LXV Congress of the Spanish Society of Digestive Diseases, Granada (Spain), June 2006.


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