It has been suggested that the concentration of L-arginine in the pregnant plasma, activity and levels of eNOS which is constitutively expressed, but not the inducible NOS are altered in endothelial cells and play critical roles in pathogenesis of preeclampsia including vascular stress and inflammatory processes [9], [14], [15], since the low availability of L-arginine uncouples eNOS activity, decreases NO production and increases eNOS-dependent superoxide generation [9], [15]. This evidence concerns the gene NOS2 and preeclampsia.