Endothelium-dependent coronary vasodilatation requires NADPH oxidase-derived reactive oxygen species.

ABSTRACT:

Objective

To determine the functional significance of physiological reactive oxygen species (ROS) levels in endothelium-dependent nitric oxide (NO)-mediated coronary vasodilatation.

Methods and results

Endothelium-derived NO is important in regulating coronary vascular tone. Excess ROS have been shown to reduce NO bioavailability, resulting in endothelial dysfunction and coronary diseases. NADPH oxidase is a major source of ROS in endothelial cells (ECs). By using lucigenin-based superoxide production and dichlorfluorescein diacetate (DCFH-DA) fluorescence-activated cell sorter assays, we found that mouse heart ECs from NADPH oxidase-knockdown (p47(phox-/-)) animals have reduced NADPH oxidase activity (>40%) and ROS levels (>30%) compared with wild-type mouse heart ECs. Surp

SUBMITTER: Feng J 

PROVIDER: S-EPMC2924465 | biostudies-literature | 2010 Sep

REPOSITORIES: biostudies-literature