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Articles in PresS, published online ahead of print October 9, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00250.2002
Submitted on May 30, 2002
Accepted on September 11, 2002
1 Department of Biomedical Sciences, Hokkaido University, Graduate School of Veterinary Medicine, Sapporo, Hokkaido, Japan
* To whom correspondence should be addressed. E-mail: torui{at}vetmed.hokudai.ac.jp.
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 perifused 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. 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.
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