Functional studies have shown that a chronic increase in cerebrospinal fluid (CSF) [Na+] by either intracerebroventricular (icv) infusion of Na+-rich artificial CSF (aCSF) or high-salt diet in genetic models of salt-sensitive hypertension activates in the brain a mineralocorticoid receptor (MR) – epithelial sodium channel (ENaC) – endogenous ouabain (EO) pathway which plays an important role in the CSF [Na+]↑ or high-salt diet-induced sympathetic hyperactivity and hypertension (for review Blaustein et al. This evidence concerns the gene NR3C2 and hypertensive disorder.