Facilitation by a hERG blocker is induced by pore opening and operates by pore reopening
K. Furutani, R. Kawano, M. Ichiwara, R. Adachi, C. E. Clancy, J. T. Sack, S. Kita
Abstract
A drug that blocks the cardiac myocyte voltage-gated K+ channels encoded by the human Ether-a-go-go-Related Gene (hERG) carries a potential risk of long QT syndrome and life-threatening cardiac arrhythmia, including Torsade de Points. Interestingly, certain hERG blockers can also facilitate hERG activation to increase hERG currents, which may reduce proarrhythmic potential. However, the molecular mechanism involved in the facilitation effect of hERG blockers remains unclear. The hallmark feature of the facilitation effect by hERG blockers is that a depolarizing preconditioning pulse shifts voltage-dependence of hERG activation to more negative voltages. Here we utilize a D540K hERG mutant to study the mechanism of the facilitation effect. D540K hERG is activated by not only depolarization but also hyperpolarization. This unusual gating property of the D540K hERG channel enables testing of hypotheses about the mechanism by which voltage induces facilitation of hERG by blockers. With D540K hERG, we find that nifekalant, a hERG blocker and Class III antiarrhythmic agent, facilitates not only current activation by depolarization but also current activation by hyperpolarization. Our results indicate that induction of facilitation is coupled to pore opening, not voltage per se. We propose that a gated-access mechanism is involved in the voltage-dependence of induction of facilitation. This study provides a molecular mechanism for modulation of hERG channels by nifekalant, a clinically important antiarrhythmic agent. Significance statementNifekalant is a clinically important antiarrhythmic agent and a hERG blocker which can also facilitate voltage-dependent activation of hERG channels after a preconditioning pulse. Here we show that the mechanism of action of the preconditioning pulse is to open a conductance gate to enable drug access to a facilitation site. Moreover, we find that facilitation increases hERG currents by altering pore dynamics, rather than acting through voltage sensors.
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