Fig. 4. Effects of isoflurane on pinacidil-activated IKATP. Whole cell current monitored during a 100-ms test pulse to 0 mV from a −40-mV holding potential was recorded in control, in 5 μm pinacidil, and in pinacidil + 0.6 mm isoflurane. (Top ) The inhibition of the isoflurane-potentiated current by 500 nm glibenclamide. (Bottom ) The reversibility of the isoflurane effect on pinacidil-activated IKATP. Traces are sequentially shown at the time depicted. The time t = 0 min denotes the recording of current during control conditions immediately prior to application of pinacidil. Note that the holding current at −40 mV also increased due to activation of IKATPby pinacidil and by pinacidil + isoflurane.

Fig. 4. Effects of isoflurane on pinacidil-activated IKATP. Whole cell current monitored during a 100-ms test pulse to 0 mV from a −40-mV holding potential was recorded in control, in 5 μm pinacidil, and in pinacidil + 0.6 mm isoflurane. (Top ) The inhibition of the isoflurane-potentiated current by 500 nm glibenclamide. (Bottom ) The reversibility of the isoflurane effect on pinacidil-activated IKATP. Traces are sequentially shown at the time depicted. The time t = 0 min denotes the recording of current during control conditions immediately prior to application of pinacidil. Note that the holding current at −40 mV also increased due to activation of IKATPby pinacidil and by pinacidil + isoflurane.

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