In this study we have investigated the voltage dependence of ATP-dependent K+ current (IK(ATP)) in atrial and ventricular myocytes from hearts of adult rats and in CHO cells expressing Kir6.2 and SUR2A. The current–voltage relation of 2,4-dinitrophenole (DNP)-induced IK(ATP) in atrial myocytes and expressed current in CHO cells was linear in a voltage range between 0 and −100 mV. In ventricular myocytes, the background current–voltage relation of which is dominated by a large constitutive inward rectifier (IK1), the slope conductance of IK(ATP) was reduced at membrane potentials negative to EK (around −50 mV), resulting in an outwardly rectifying I–V relation. Overexpression of Kir2.1 by adenoviral gene transfer, a subunit contributing to IK1 channels, in atrial myocytes resulted in a large IK1-like background current. The I–V relation of IK(ATP) in these cells showed a reduced slope conductance negative to EK similar to ventricular myocytes. In atrial myocytes with an increased background inward-rectifier current through Kir3.1/Kir3.4 channels (IK(ACh)), irreversibly activated by intracellular loading with GTP-γ-S, the I–V relation of IK(ATP) showed a reduced slope negative to EK, as in ventricular myocytes and atrial myocytes overexpressing Kir2.1. It is concluded that the voltage dependencies of membrane currents are not only dependent on the molecular composition of the charge-carrying channel complexes but can be affected by the activity of other ion channel species. We suggest that the interference between inward IK(ATP) and other inward rectifier currents in cardiac myocytes reflects steady-state changes in K+ driving force due to inward K+ current
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