Neuronal nitric oxide synthase regulation of calcium cycling in ventricular cardiomyocytes is independent of Ca_v1.2 channel modulation under basal conditions.

ABSTRACT: Neuronal nitric oxide synthase (nNOS) is considered a regulator of Ca_v1.2 L-type Ca²⁺ channels and downstream Ca²⁺ cycling in the heart. The commonest view is that nitric oxide (NO), generated by nNOS activity in cardiomyocytes, reduces the currents through Ca_v1.2 channels. This gives rise to a diminished Ca²⁺ release from the sarcoplasmic reticulum, and finally reduced contractility. Here, we report that nNOS inhibitor substances significantly increase intracellular Ca²⁺ transients in ventricular cardiomyocytes derived from adult mouse and rat hearts. This is consistent with an inhibitory effect of nNOS/NO activity on Ca²⁺ cycling and contractility. Whole cell currents through L-type Ca²⁺ channels in r

SUBMITTER: Ebner J 

PROVIDER: S-EPMC6960210 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature