NAD⁺ reduces ventricular arrhythmias by inhibiting I_NaL and I_to in mice

Objective: Decreased nicotinamide adenine dinucleotide (NAD+) levels are a common feature of cardiovascular diseases, exogenous NAD+ can also block myocardial hypertrophy responses in vivo and in vitro. A few studies have reported the anti-arrhythmic effects of NAD + and late sodium current (I NaL ) contributes to the occurrence of arrhythmias, there are currently no reports on the effect of NAD + on I NaL . This study aims to explore whether NAD + exerts anti-arrhythmic effects by inhibiting I NaL . Methods: Whole cell patch clamp technology was applied to investigate the effects of NAD + on I NaL , transient outward potassium current (I to ) in mice ventricular myocytes. The electrocardiograms (ECGs) of the mice was recorded for the anti-arrhythmic effect induced by Anemone toxinⅡ (ATXⅡ, I NaL specific opener) of NAD + .