In response to heat-stable enterotoxin of Vibrio cholerae non-O1, the initial rise of cytosolic 2 entry to the cell as assessed by Mn 2 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 [Ca 2 ]i response. Addition of toxin to the fura-2-loaded cells, preincubated with lanthanum chloride, resulted in reduction of [Ca 2 ]i level with a short duration of irregular sustained phase further suggesting that the influx of Ca 2 across the plasma membrane might be through the calcium channel. ß
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