Calcium-dependent chloride current activated by hyposmotic stress in rat lacrimal acinar cells.

We have identified a whole-cell Cl- current activated by hyposmotic stress in rat lacrimal acinar cells using the patch-clamp technique. Superfusion of isolated single cells with hyposmotic solution (80% of control osmolarity) caused a gradual increase of the current, which was reversed on return to the control solution. The current-voltage relationship showed outward rectification, and the current showed time and voltage dependence: slowly activated by depolarizing voltages and rapidly inactivated by hyperpolarizing voltages. The increase in current was not observed when intracellular Ca2+ was chelated with EGTA. It was also inhibited by the absence of extracellular Ca2+, or the presence of gadolinium ions (20 microM Gd3+). We conclude that in rat lacrimal acinar cells hyposmotic stress activates Ca(2+)-dependent Cl- channels as a result of Ca2+ influx through a Gd(3+)-sensitive pathway. The Cl- channels involved appear to be indistinguishable from those activated by muscarinic stimulation. The inhibitory effect of Gd3+ suggests that stretch-activated nonselective cation channels may be responsible for the Ca2+ influx.