Kir2.3 knock-down decreases IK1 current in neonatal rat cardiomyocytes

Inward rectifier potassium Kir2.x channels mediate cardiac inward rectifier potassium currents (IK1). As a subunit of Kir2.x, the physiological role of Kir2.3 in native cardiomyocytes has not been reported. This study shows that Kir2.3 knock-down remarkably down-regulates Kir2.3 expression (Kir2.3 protein was reduced to 19.91 ± 3.24% on the 2nd or 3rd day) and IK1 current densities (at −120 mV, control vs. knock-down: −5.03 ± 0.24 pA/pF, n = 5 vs. −1.16 ± 0.19 pA/pF, n = 7, P < 0.001) in neonatal rat cardiomyocytes. The data suggest that Kir2.3 plays a potentially important role in IK1 currents in neonatal rat cardiomyocytes.