ACE and endothelial dysfunction: Experimental data suggest that the RAS modulates the atherosclerotic process, and that AT exerts proinflammatory actions in the vascular wall, which induce the production of reactive oxygen species and hydroxyl radicals, cytokines, and adhesion molecules.[22–25] ACE-Is could provide neuroprotection via blockade of AT-mediated endothelial dysfunction, lipid peroxidation, and subsequent oxidative stress and vascular smooth muscle intracellular calcium accumulation and hypertrophy.[26–27]