CAPON modulates neuronal calcium handling and cardiac sympathetic neurotransmission during dysautonomia in hypertension.

ABSTRACT: Genome-wide association studies implicate a variant in the neuronal nitric oxide synthase adaptor protein (CAPON) in electrocardiographic QT variation and sudden cardiac death. Interestingly, nitric oxide generated by neuronal NO synthase-1 reduces norepinephrine release; however, this pathway is downregulated in animal models of cardiovascular disease. Because sympathetic hyperactivity can trigger arrhythmia, is this neural phenotype linked to CAPON dysregulation? We hypothesized that CAPON resides in cardiac sympathetic neurons and is a part of the prediseased neuronal phenotype that modulates calcium handling and neurotransmission in dysautonomia. CAPON expression was significantly reduced in the stellate ganglia of spontaneously hypertensive rats before the development of hypertension

SUBMITTER: Lu CJ 

PROVIDER: S-EPMC4487208 | biostudies-literature | 2015 Jun

REPOSITORIES: biostudies-literature