Nitric oxide down-regulates voltage-gated Na⁺ channel in cardiomyocytes possibly through S-nitrosylation-mediated signaling.

ABSTRACT: Nitric oxide (NO) is produced from endothelial cells and cardiomyocytes composing the myocardium and benefits cardiac function through both vascular-dependent and-independent effects. This study was purposed to investigate the possible adverse effect of NO focusing on the voltage-gated Na⁺ channel in cardiomyocytes. We carried out patch-clamp experiments on rat neonatal cardiomyocytes demonstrating that NOC-18, an NO donor, significantly reduced Na⁺ channel current in a dose-dependent manner by a long-term application for 24 h, accompanied by a reduction of Nav1.5-mRNA and the protein, and an increase of a transcription factor forkhead box protein O1 (FOXO1) in the nucleus. The effect of NOC-18 on the Na⁺ channel was blocked by an inhibitor of thiol oxidati

SUBMITTER: Wang P 

PROVIDER: S-EPMC8163867 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature