Evidence of calcium influx across the plasma membrane depends upon the initial rise of cytosolic calcium with activation of IP3 in rat enterocytes by heat-stable enterotoxin of Vibrio cholerae non-O1

Abstract In response to heat-stable enterotoxin of Vibrio cholerae non-O1, the initial rise of cytosolic Ca2+ occurred with activation of IP3. Chelation of extracellular Ca2+ with EGTA and suspension of cells in Ca2+ free buffer both demonstrated the involvement of internal stores in the rise of [Ca2+]i. Cells pretreated with dantrolene resulted in decrease of [Ca2+]i response which suggested that the rise of intracellular level of Ca2+ was mostly due to the mobilization from IP3 sensitive stores. When the cytosolic Ca2+ was chelated by loading the cells with BAPTA, NAG-ST could not induce Ca2+ entry to the cell as assessed by Mn2+ quenching of fura-2 fluorescence which suggested that calcium influx across the plasma membrane depends upon initial rise of this bivalent cation that maintained the sustained phase of [Ca2+]i response. Addition of toxin to the fura-2-loaded cells, preincubated with lanthanum chloride, resulted in reduction of [Ca2+]i level with a short duration of irregular sustained phase further suggesting that the influx of Ca2+ across the plasma membrane might be through the calcium channel.