Sodium leak through K2P potassium channels and cardiac arrhythmia, an emerging theme

In this issue of EMBO Molecular Medicine, Decher et al (2017) identify a point mutation in the K2P2 (TREK-1) potassium (K⁺) channel that changes function in just those ways expected to predispose to right ventricular outflow tract (RVOT) ventricular tachycardia (VT) in the patient they study. Whereas wild-type channels are selective for K⁺ and inhibited by β-adrenergic stimulation, mutant I267T channels pass sodium (Na⁺) into the cells, even during β-adrenergic stimulation, and are more active in response to membrane stretch, changes predicted to enhance cardiac myocyte excitability. The report contributes to accumulating evidence for Na⁺ leak via K2P channels in association with normal development (Thomas et al, 2008), acquired arrhythmia (Ma et al, 2011), and now a missense mutation. Decher et al (2017) both inform and direct us toward interesting opportunities for further investigation.

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