NF-kappaB-dependent transcriptional regulation of the cardiac scn5a sodium channel by angiotensin II.

ABSTRACT: Angiotensin II (ANG II) increases oxidative stress and is associated with increased risk of sudden cardiac death. The cardiac Na(+) channel promoter contains elements that confer redox sensitivity. We tested the hypothesis that ANG II-mediated oxidative stress may modulate Na(+) channel current through altering channel transcription. In H9c2 myocytes treated for 48 h with ANG II (100 nmol/l) or H(2)O(2) (10 micromol/l) showed delayed macroscopic inactivation, increased late current, and 59.6% and 53.8% reductions in Na(+) current, respectively (P < or = 0.01). By quantitative real-time RT-PCR, the cardiac Na(+) channel (scn5a) mRNA abundance declined by 47.3% (P < 0.01) in H9c2 myocytes treated for 48 h with 100 nmol/l ANG II. A similar change occurred with 20 micromol/l H(2)O(2) (46.9%, P

SUBMITTER: Shang LL 

PROVIDER: S-EPMC3150844 | biostudies-literature | 2008 Jan

REPOSITORIES: biostudies-literature