K_V4.3 Expression Modulates Na_V1.5 Sodium Current.

ABSTRACT: In cardiomyocytes, the voltage-gated transient outward potassium current (I_to) is responsible for the phase-1 repolarization of the action potential (AP). Gain-of-function mutations in KCND3, the gene encoding the I_to carrying K_V4.3 channel, have been associated with Brugada syndrome (BrS). While the role of I_to in the pro-arrhythmic mechanism of BrS has been debated, recent studies have suggested that an increased I_to may directly affect cardiac conduction. However, the effects of an increased I_to on AP upstroke velocity or sodium current at the cellular level remain unknown. We here investigated the consequences of K_V4.3 overexpression on Na_V1.5 current and consequent sodium channel availabilit

SUBMITTER: Portero V 

PROVIDER: S-EPMC5857579 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature