Mediation of H2O2-induced vascular relaxation by endothelium-derived relaxing factor.

We investigated the effects of H2O2 generated by glucose (G) and glucose glucose oxidase (GO) on the isolated rabbit aorta suspended in Krebs-Ringer solution. H2O2 produced contraction in small concentration and relaxation followed by contraction in large concentration. Contraction produced by large concentration was smaller than that produced by small concentration of H2O2. Relaxation was prevented by deendothelialization or NG-monomethyl-L-arginine, an inhibitor of nitric oxide synthesis. These results suggest that H2O2 in large concentrations produces relaxation followed by contraction, and that the relaxation is endothelium-dependent and is mediated by nitric oxide, an endothelium-derived relaxing factor.