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¹ Department of Physiology, Ruhr-University Bochum, D-44780 Bochum, Germany

In this study we have investigated the voltage dependence of ATP-dependent K⁺ current (I_K(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 I_K(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 (I_K1), the slope conductance of I_K(ATP) was reduced at membrane potentials negative to E_K (around –50 mV), resulting in an outwardly rectifying I–V relation. Overexpression of Kir2.1 by adenoviral gene transfer, a subunit contributing to I_K1 channels, in atrial myocytes resulted in a large I_K1-like background current. The I–V relation of I_K(ATP) in these cells showed a reduced slope conductance negative to E_K similar to ventricular myocytes. In atrial myocytes with an increased background inward-rectifier current through Kir3.1/Kir3.4 channels (I_K(ACh)), irreversibly activated by intracellular loading with GTP--S, the I–V relation of I_K(ATP) showed a reduced slope negative to E_K, 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 I_K(ATP) and other inward rectifier currents in cardiac myocytes reflects steady-state changes in K⁺ driving force due to inward K⁺ current.

(Received 3 August 2004; accepted after revision 27 September 2004; first published online 30 September 2004)
Corresponding author L. Pott: Department of Physiology, Ruhr-University Bochum, D-44780 Bochum, Germany Email: lutz.pott{at}rub.de

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