Hyper-activation of ACE/Ang II/AT1 axis or dysregulation of ACE-2/Angiotensin 1–7 (Ang 1–7) MasR axis potentially aggravates endothelial dysfunction, fibrosis, oxidative stress, monocyte/macrophage cell infiltration to perivascular tissue, in the kidney and heart, leading to blood pressure rise. This evidence concerns the gene ACE and endothelial dysfunction.