Abstract
Small-conductance Ca2+-activated K+ (SK) channels are predominantly expressed in the atria, thus offering a unique therapeutic target for atrial fibrillation (AF) independent of ventricular function. Several studies have reported remodeling of SK channels in AF, whereby SK current is increased during AF-induced remodeling in several animal models. Nevertheless, data on SK current (ISK) in atrial myocytes from patients remain scarce, and the AF-associated changes are controversial. Both upregulation and downregulation have been reported in chronic AF vs. normal sinus rhythm, accompanied by increased or decreased action potential duration (APD) lengthening by SK-channel inhibition. A potential confounding factor is the observation that sex-specific differences exist in ISK function in the ventricles, which could also be present in the atria, though this remains unknown.
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