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J Physiol Volume 508, Number 1, 23-30, April 1, 1998
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The Journal of Physiology (1998), 508.1, pp. 23-30
© Copyright 1998 The Physiological Society

Cystic fibrosis transmembrane conductance regulator mediates sulphonylurea block of the inwardly rectifying K+ channel Kir6.1

Ayako Ishida-Takahashi, Hideo Otani, Chiaki Takahashi *, Takashi Washizuka, Keiko Tsuji, Makoto Noda *, Minoru Horie and Shigetake Sasayama

Departments of Cardiovascular Medicine and * Molecular Oncology, Kyoto University Graduate School of Medicine, Kyoto 606-01, Japan

  1. Recombinant ATP-sensitive K+ channels (KATP channels) were heterologously expressed in the NIH3T3 mouse cell line, and the electrophysiological properties were studied using patch-clamp techniques.

  2. The NIH3T3 cell lines transfected with the inwardly rectifying K+ channel Kir6.1 alone or with both Kir6.1 and cystic fibrosis transmembrane conductance regulator (CFTR) exhibited time-independent K+ currents with weak inward rectification. In contrast, no measurable K+ conductance was observed in mock-transfected cells or in cells transfected with CFTR alone. Regardless of co-transfection with Kir6.1, the transfection with CFTR produced a Cl- conductance that was activated by cell dialysis with cAMP (1 mM). The conductance was reversibly suppressed by glibenclamide (30 µM).

  3. Whole-cell currents at +60 mV were blocked in a concentration-dependent manner by Ba2+ ions with similar IC50 values: 89·3 ± 23·3 µM (Kir6.1 alone) and 67·3 ± 24·9 µM (Kir6.1-CFTR).

  4. The currents recorded from Kir6.1-transfected cells were not affected by glibenclamide, whereas glibenclamide did inhibit the conductance expressed in cells co-transfected with CFTR (IC50 = 35·9 ± 6·6 µM).

  5. In the cell-attached mode with a 150 mM K+ pipette solution, both Kir6.1- and Kir6.1-CFTR-transfected cells displayed a class of K+ channels showing weak inward rectification and a slope conductance of 50·7 ± 1·0 and 52·4 ± 4·9 pS, respectively.

  6. In the inside-out mode, the single-channel currents recorded from both types of cells were not inhibited by intracellular ATP (1 mM). However, glibenclamide was found to block the single-channel activities in the co-transfected cells.




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