The Functional Consequences of Sodium Channel NaV1.8 in Human Left Ventricular Hypertrophy

Abstract

We show for the first time that the neuronal sodium channel Na_V 1.8 is up-regulated on mRNA and protein level in the human hypertrophied myocardium. Furthermore, inhibition of Na_V 1.8 reduced augmented I_NaL , abbreviated the action potential duration, and decreased the SR-Ca²⁺ leak. The findings of our study suggest that Na_V 1.8 could be a promising antiarrhythmic therapeutic target and merits further investigation.