SK4/IK1-like channels mediate TEA-insensitive, Ca2+-activated K+ currents in bovine parotid acinar cells.

Although Ca(2+)-activated K(+) (K(Ca)) channels distinct from maxi-K(+) channels have been suggested to contribute to muscarinically stimulated K(+) currents in salivary acinar cells, the molecular nature of the channels is unclear. Using electrophysiological and RT-PCR techniques, we have now investigated the involvement of SK4/IK1-like channels in native K(Ca) currents in bovine parotid acinar (BPA) cells. Ca(2+)-dependent K(+) efflux from perfused bovine parotid tissues was not inhibited by a maxi-K(+) channel blocker, tetraethylammonium (TEA). Whole cell recordings from BPA cells showed a TEA-insensitive K(Ca) conductance, which was highly permeable to Rb(+). In inside-out macropatches, TEA-insensitive Rb(+) currents were activated by Ca(2+) with half-maximal values of 0.4 microM. 1-Ethyl-2-benzimidazolinone (1-EBIO) increased the Ca(2+) sensitivity of the currents. The calmodulin antagonists trifluoperazine, calmidazolium, and W-7 inhibited the Ca(2+)-activated Rb(+) currents. In outside-out macropatches, Ca(2+)-activated Rb(+) currents were inhibited by Ba(2+), quinine, clotrimazole, and charybdotoxin but not by d-tubocrarine or apamin. RT-PCR analysis showed transcripts of SK4/IK1 in BPA cells. These results collectively suggest that SK4/IK1-like channels mediate the native K(Ca) currents in BPA cells.