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Korean J Gastroenterol. 2000 May;35(5):539-545. Korean. Original Article.
Sim SS , Choi JC , Kim MS , Kim CJ , Jo YH .
Abstract

BACKGROUND/AIMS: The mechanism of ethanol in contraction of gastric smooth muscle still remains unclear. To investigate underlying mechanism of ethanol in tonic contraction, we measured isometric contractions of cat gastric smooth muscle using various Ca2+antagonists and protein kinase inhibitors. METHODS: Circular muscle strips (2.0x0.2 cm) were prepared from the fundus of stomach to measure isometric contraction, and their contractions were recorded in a cylinder-shaped chamber filled with Krebs-Ringer solution (pH 7.4, temperature 36C degrees) bubbled with 5% CO2 in O2. RESULTS: Ethanol induced tonic contraction in a dose-dependent manner. EGTA inhibited dose-dependently the contraction induced by 2% ethanol. Ethanol-induced contraction was not inhibited by verapamil, diltiazem or TMB-8. However, econazole (a blocker of receptor-operated Ca2+channel) significantly inhibited ethanol-induced contraction. Ethanol-induced contraction was significantly inhibited by 10 micrometer bisindolylmaleimide and 50 micrometer genistein, but not by 50 micrometer W-7 and 30 micrometer trifluoperazine. One micrometer PMA (Protein kinase C activator) augmented ethanol-induced contraction, whereas tyrosine phosphatase inhibitors such as BTH, BPA and vanadate, did not. CONCLUSIONS: From the above results, it is suggested that ethanol-induced contraction is mediated by protein kinase C and tyrosine kinase, and the influx of extracellular Ca2+ induced by ethanol is mediated via econazole-sensitive Ca2+channel.

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