Figure 1.
The activation of endothelial nitric oxide synthase (eNOS) may be induced by shear stress, estrogens, or increase of intracellular Ca2+ concentration and may be inhibited, mainly during aging physiopathological process, by oxidative stress and reduction of Sirtuin 1 activity and of estrogens level. In healthy endothelium, eNOS plays multiple functions, such as nitric-oxide vasodilation and inhibition of platelet aggregation and may induce endothelial progenitor cells activation and functions.