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

Institute of Cardiovascular Diseases, Hubei Province Key Laboratory of Occupational Hazard Identification and Control, School of Medicine, Wuhan University of Science and Technology, Wuhan 430065, China.

^* Correspondence to: Antao Luo, PhD Email: lat78@126.com.

Abstract

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⁺.