Abstract: | This study examines theCa2+ influx-dependent regulationof the Ca2+-activatedK+ channel(KCa) in human submandibulargland (HSG) cells. Carbachol (CCh) induced sustained increases in theKCa current and cytosolic Ca2+ concentration(Ca2+]i),which were prevented by loading cells with1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA). Removal of extracellularCa2+ and addition ofLa3+ orGd3+, but notZn2+, inhibited the increases inKCa current andCa2+]i.Ca2+ influx during refill (i.e.,addition of Ca2+ to cells treatedwith CCh and then atropine inCa2+-free medium) failed to evokeincreases in the KCa current but achieved internal Ca2+ storerefill. When refill was prevented by thapsigargin,Ca2+ readdition induced rapidactivation of KCa. These dataprovide further evidence that intracellularCa2+ accumulation provides tightbuffering ofCa2+]iat the site of Ca2+ influx (H. Mogami, K. Nakano, A. V. Tepikin, and O. H. Petersen. Cell 88: 49-55, 1997). We suggestthat the Ca2+ influx-dependentregulation of the sustained KCacurrent in CCh-stimulated HSG cells is mediated by the uptake ofCa2+ into the internalCa2+ store and release via theinositol 1,4,5-trisphosphate-sensitive channel. |