NOS2 and septic shock: In addition, in sepsis, endotoxin and its metabolites can stimulate increased expression and activity of inducible nitric oxide synthase (iNOS) in a variety of cells [45], inducing the generation of large amounts of NO by vascular endothelial cells, which can generate ONOO-radicals during oxidation, causing oxidation of membrane lipids, endothelial damage, and vasodilation, leading to a decrease in blood pressure and tissue perfusion, and inducing septic shock.