Physiological effects of RAS are achieved through the interaction of counterbalancing activity pathways: “pathophysiological” ACE/ANGII/AT1R, whose activation is associated with hypertension, oxidative stress, hypertrophy, fibrosis and inflammation, and “protective” ACE/ANGII/AT2R, which has the opposite function, including hypotensive and anti-inflammatory effects (18). Here, ACE is linked to Hypertension.