EDN1 and endothelial dysfunction: In addition to NO as one critical factor in endothelial function, enhanced activities and levels of ET1 also were related to endothelial dysfunction by stimulating nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived ROS production, which inhibits NO-mediated endothelial relaxation and mediating ETA receptors to blunt NO relaxant responses (26).