Fig. 6. Effects of etomidate on the channel activities of the truncated isoform of inwardly rectifying potassium channel 6.2 (Kir6.2ΔC36), which can form functional adenosine triphosphate (ATP)–sensitive potassium channels in the absence of sulfonylurea receptor molecules, in the inside-out configuration. Membrane potentials were clamped at −60 mV. (  A ) Representative examples of Kir6.2ΔC36 currents obtained before and after application of etomidate (10−5m). The periods of etomidate treatment are marked with  horizontal bars . (  B ) The percentage of inhibition of channel activity of Kir6.2ΔC36 channel alone and Kir6.2ΔC36 channel bearing the K185Q mutation by intracellular etomidate (10−5m) and ATP (10−3m). Each  horizontal bar represents measurements from 8 patches (mean ± SD). *  P < 0.05  versus Kir6.2ΔC36 channel alone. 

Fig. 6. Effects of etomidate on the channel activities of the truncated isoform of inwardly rectifying potassium channel 6.2 (Kir6.2ΔC36), which can form functional adenosine triphosphate (ATP)–sensitive potassium channels in the absence of sulfonylurea receptor molecules, in the inside-out configuration. Membrane potentials were clamped at −60 mV. (  A ) Representative examples of Kir6.2ΔC36 currents obtained before and after application of etomidate (10−5m). The periods of etomidate treatment are marked with  horizontal bars . (  B ) The percentage of inhibition of channel activity of Kir6.2ΔC36 channel alone and Kir6.2ΔC36 channel bearing the K185Q mutation by intracellular etomidate (10−5m) and ATP (10−3m). Each  horizontal bar represents measurements from 8 patches (mean ± SD). *  P < 0.05  versus Kir6.2ΔC36 channel alone. 

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