The Involvement of Calcium Mobilization in the Calcium-Activated Potassium Currents Activated by Hyposmotic Swelling in Gastric Antral Circular Myocytes of the Guinea-Pig.

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Abstract
In our study of the effects of hyposmotic swelling on the Ca(2+)-activated potassium currents [I(K(Ca))] and its mechanism, we employed the whole-cell patch clamp technique using the gastric antral circular myocytes of the guinea-pig. Hyposmotic swelling efficiently increased I(K(Ca)), and the extent of changes in I(K(Ca)) was sharply dependent on the osmolarity of the perfusion solutions. When the calcium-free solution (EGTA 10 microM added in calcium-free solution) was superfused, I(K(Ca)) was not increased by the hyposmotic swelling. Gadolinium (Gd(3+)) 100 nM, a blocker of the stretch-activated nonselective cation channel, blocked the activation of I(K(Ca)) induced by hyposmotic swelling, but nicardipine 5 microM (the L-type calcium channel blocker) did not. Heparin 3 mg/ml, a potent inhibitor of inositol triphosphate receptor (InsP(3)R), did not inhibit the response, and caffeine 1 mM (the agonist for calcium-induced calcium release [CICR]) imitated the effect of hyposmotic swelling. Ryanodine (15 microM), markedly inhibited the effect. These results suggest that hyposmotic swelling activates I(K(Ca)), and the activation is associated with CICR, which is triggered by extracellular calcium influx through the stretch-activated channel (SA channel).