These were observable as the spontaneous release of NO [67,68], as a counteraction of the adverse effect of a NOS blockade (i.e., L-NAME hypertension and pro-thrombotic effect), a counteraction of the adverse effect of NOS overstimulation (i.e., L-arginine hypotension and anti-thrombotic effect) [67,69], as control of vasomotor tone and as the activation of the Src-Caveolin-1-eNOS pathway [60,61]. The gene discussed is NOS2; the disease is hypertensive disorder.