Figure 5. Primaquine reduces apamin‐sensitive I _K,Ca in mouse atrial myocytes.

A, Ca²⁺‐activated K⁺ currents recorded from mouse atrial myocytes, before and after application of 100 pm apamin. Current–voltage relationship of Ca²⁺‐activated K⁺ currents before (black line) and after apamin (blue line). Atrial myocytes were pretreated with 50 μm primaquine or control. Currents were elicited using a voltage‐ramp protocol from a holding potential of −55 mV from −120 mV to +60 mV using a slope of 0.09 mV ms⁻¹. B, summary data for apamin‐sensitive current density recorded at −120 and +60 mV were plotted in a bar graph. ^* P = 0.01, ^** P < 0.0000001, (n = 6). C and D, acute effects of primaquine (50 μm) in HEK 293 cells co‐expressing SK2 and α‐actinin2. There was no change in the apamin‐sensitive currents after 15 min application of primaquine. Similar data were obtained from 5 separate cells. E, control experiments were performed by recording the currents from non‐transfected HEK293 cells. In addition, consistent with our previous findings, co‐expression of SK2 channels with α‐actinin2 significantly increased the apamin‐sensitive currents (100 pm of apamin). F, summary data showing I _K,Ca density at −120 and +60 mV from HEK 293 cells expressing SK2 alone or SK2 and α‐actinin2 (n = 6, ^* P < 0.05). G, a schematic diagram depicting the possible steps where α‐actinin2 and FLNA may enhance the anterograde trafficking of SK2 channels to the membrane.