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The functional consequences of sodium channel NaV 1.8 in human left ventricular hypertrophy.


ABSTRACT:

Aims

In hypertrophy and heart failure, the proarrhythmic persistent Na+ current (INaL ) is enhanced. We aimed to investigate the electrophysiological role of neuronal sodium channel NaV 1.8 in human hypertrophied myocardium.

Methods and results

Myocardial tissue of 24 patients suffering from symptomatic severe aortic stenosis and concomitant significant afterload-induced hypertrophy with preserved ejection fraction was used and compared with 12 healthy controls. We performed quantitative real-time PCR and western blot and detected a significant up-regulation of NaV 1.8 mRNA (2.34-fold) and protein expression (1.96-fold) in human hypertrophied myocardium compared with healthy hearts. Interestingly, NaV 1.5 protein express

SUBMITTER: Ahmad S 

PROVIDER: S-EPMC6352890 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature