Considering the impact on vasodilation, administration of L-NAME and its conversion into the active N(omega)-nitro-L-arginine (L-NOARG) in turn inhibited eNOS, leading to the deficiency of the potent vasodilating NO and subsequently the occurrence of systemic vasoconstriction and hypertension (Pfeiffer et al., 1996; Hopkins et al., 2013). This evidence concerns the gene NOS3 and hypertensive disorder.