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Am J Physiol Cell Physiol 284: C127-C144, 2003. First published October 9, 2002; doi:10.1152/ajpcell.00250.2002
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Vol. 284, Issue 1, C127-C144, January 2003

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

T. Takahata, M. Hayashi, and T. Ishikawa

Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan

Although Ca2+-activated K+ (KCa) 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 KCa currents in bovine parotid acinar (BPA) cells. Ca2+-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 KCa conductance, which was highly permeable to Rb+. In inside-out macropatches, TEA-insensitive Rb+ currents were activated by Ca2+ with half-maximal values of 0.4 µM. 1-Ethyl-2-benzimidazolinone (1-EBIO) increased the Ca2+ sensitivity of the currents. The calmodulin antagonists trifluoperazine, calmidazolium, and W-7 inhibited the Ca2+-activated Rb+ currents. In outside-out macropatches, Ca2+-activated Rb+ currents were inhibited by Ba2+, 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 KCa currents in BPA cells.

patch clamp; salivary secretion; HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> transport


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