Korean J Gastroenterol.
2000 May;35(5):539-545.
Effects of Ca2+ Antagonists and Protein Kinase Inhibitors
on Ethanol-Induced Contraction of Cat Gastric Smooth Muscle
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.