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. 2013 Oct 14;35(1):58–64. doi: 10.1038/aps.2013.122

Figure 1.

Figure 1

Acute MGO treatment led to activation of the Kir6.1/SUR2B channel. (A) The Kir6.1/SUR2B channel was expressed in HEK293 cells. Whole-cell currents were recorded from cells two days after transfection in a voltage-clamp configuration. MGO (0.3–3 mmol/L) treatment led to the activation of Kir6.1/SUR2B currents in a concentration-dependent manner. Pinacidil (Pin, 10 μmol/L), a KATP channel-specific opener, further opened the channel. The application of the KATP channel-specific inhibitor glibenclamide (Glib, 10 μmol/L) dramatically reduced the current. For quantitative analysis, the effect of MGO was normalized between the baseline current and the current activated by 10 μmol/L Pin. In the presence of Glib (10 μmol/L), the effect of the higher concentration of MGO (10 mmol/L) on channel activation was completely blocked. (B) The MGO-mediated channel activation was reversible. Following channel activation by MGO, washout with the bath solution returned the KATP channel currents to an almost baseline level. Glib caused a further reduction of the KATP channel currents. (C) Summary of the effect of MGO on the KATP channel currents in the presence and absence of Glib. bP<0.05. (D) Dose-response relationship between the concentration of MGO and the normalized current. Data were described by the Hill-equation with an EC50 of 1.7 mmol/L.