Nitric oxide (NO) synthase but not NO, HNO or H O mediates endothelium-dependent relaxation of resistance arteries from patients with cardiovascular disease.

Background And Purpose: Superoxide anions can reduce the bioavailability and actions of endothelium-derived NO. In human resistance-sized arteries, endothelium-dependent vasodilatation can be mediated by H O instead of NO. Here, we tested the hypothesis that in resistance arteries from patients with cardiovascular disease, endothelium-dependent vasodilatation is mediated by a reactive oxygen species and not impaired by oxidative stress.