Zw. Yang et al., Importance of extracellular Ca2+ and intracellular Ca2+ release in ethanol-induced contraction of cerebral arterial smooth muscle, ALCOHOL, 24(3), 2001, pp. 145-153
The present study was designed to investigate the roles of extracellular Ca
2+ ([Ca2+](0)) influx and intracellular free Ca2+ ([Ca2+](i)) release in et
hanol-induced contractions of isolated canine cerebral arteries and primary
cultured, cerebral vascular smooth muscle cells. Ethanol (20-200 mM) produ
ced significant contractions in isolated canine basilar arterial rings in a
concentration-dependent manner. Removal of [Ca2+](0) and pretreatment of c
anine basilar arterial rings with verapamil (an antagonist of voltage-gated
Ca2+ channels), thapsigargin (a selective antagonist of the sarcoplasmic r
eticulum Ca2+ pump), caffeine plus ryanodine (a specific antagonist of ryan
odine-sensitive Ca2+ release), or heparin (an inositol 1,4,5,-trisphosphate
[InsP(3)]-mediated Ca2+ release antagonist) markedly attenuated (-50%-80%)
ethanol-induced contractions. The absence of [Ca2+](0) and preincubation o
f primary single smooth muscle cells obtained from canine basilar arteries
with verapamil, thapsigargin, heparin, or caffeine plus ryanodine markedly
attenuated (-50%-80%) the transient and sustained elevations in [Ca2+](i) i
nduced by ethanol. Results of the present study suggest to us that both Ca2
+ influx through voltage-gated Ca2+ channels and Ca2+ release from intracel
lular stores (both InsP(3) sensitive and ryanodine sensitive) are required
for ethanol-induced contractions of isolated canine basilar arteries. (C) 2
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