These results suggest that, although the major antihypertensive effect of MP may be mediated via the upregulation of eNOS and increase in NO bioavailability, other possible mechanisms of MP such as inhibition of sympathetic over activity and inactivation of renin-angiotensin system by MP should be considered, because those two pathways can be activated by l-NAME to induce hypertension [37]. The gene discussed is NOS3; the disease is Hypertension.