SK channel blockade prevents hypoxia-induced ventricular arrhythmias through inhibition of Ca²⁺/voltage uncoupling in hypertrophied hearts

Abstract

We demonstrated that hypoxia-induced ventricular arrhythmias were mainly initiated by Ca 2+ -loaded triggered activities in hypertrophied hearts. The blockades of small-conductance Ca 2+ -activated K + channels, especially “apamin,” showed anti-arrhythmic effects by alleviation of not only action potential duration shortening but also Ca 2+ handling abnormalities, most notably the “Ca 2+ /voltage uncoupling.”