This preclinical study demonstrates that the rectification of the steady-state current in guinea-pig ventricular cells is driven by the kinetic properties of the inwardly rectifying K channel, which depend on the driving force rather than absolute membrane potential.
Currents through the inwardly rectifying K channel were studied under whole-cell clamp of collagenase-treated single ventricular cells of guinea-pigs. The inwardly rectifying K channel was fully activated by hyperpolarizing the membrane from the equilibrium potential for K+ (EK) by 30-40 mV. Following depolarization above EK, a decaying outward current was elicited. Prolongation of the hyperpolarizing prepulse increased the amplitude of the decaying outward current, with a time course similar to the increase of the inward current during the prepulse. Time-dependent changes in both outward and inward currents could be fitted with a single exponential function and were attributed to deactivation and activation of the inwardly rectifying K channel. The instantaneous current-voltage relation was almost linear, indicating that the conductance of the channel is ohmic and that the rectification of the steady-state current was due to the kinetic properties of the inwardly rectifying K channel. The activation kinetics of the channel was measured at different concentrations of K+ in both the external and internal solutions. The time constant and the steady-state activation were not a function of the absolute membrane potential value, but were dependent on the driving force.
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Saigusa et al. (1988) studied this question.
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