In rat stomach fundus, contractions induced by Ca2+ (1.8 mM) were stri
kingly potentiated by thapsigargin. This potentiation was partially in
hibited by the blockers of Ca2+ release activated channels (CRACs), mi
conazole and SK&F96365 ({1-[beta-[3-(4-methoxyphenyl)propoxy]-4- metho
xyphenethyl]-1H-imidazole, HCL}) and slightly blocked by the antagonis
t of calcium voltage-operated channels (VOCs), isradipine. In dissocia
ted cells in a 0Ca solution, thapsigargin potentiated the increase in
intracellular calcium after reintroduction of Ca2+. This potentiation
was partially reduced by the CRAC blockers, but not by the VOC blocker
s. This data suggests that calcium influx increased due to the depleti
on of intracellular calcium by thapsigargin and that this influx occur
s predominantly through CRACs. (C) 1998 Elsevier Science B.V.