MR antagonists (MRAs), highly effective agents in the treatment of refractory hypertension, also reverse the adverse effects (sodium retention, potassium loss, endothelial dysfunction, vascular inflammation, myocardial hypertrophy, and fibrosis) of hyperaldosteronism and/or activation of MRs, leading to reduced oxidative stress and collagen deposition and improved perfusion of cardiac and brain tissue [17,18,19]. This evidence concerns the gene NR3C2 and Hypertension.