Neuronal NO synthase mediates plenylephrine induced cardiomyocyte hypertrophy through facilitation of NFAT-dependent transcriptional activity.

Neuronal nitric oxide synthase (NOS1) has been consistently shown to be the predominant isoform of NOS and/or NOS-derived NO that may be involved in the myocardial remodeling including cardiac hypertrophy. However, the direct functional contribution of NOS1 in this process remains to be elucidated. Therefore, in the present study, we attempted to use silent RNA and adenovirus mediated silencing or overexpression to investigate the role of NOS1 and the associated molecular signaling mechanisms during OKphenylephrine (PE)-induced cardiac hypertrophy growth in neonatal rat ventricular cardiomyocytes (NRVMs).