Overall, elevated [Na+]CSF is now thought to cause sustained activation of central angiotensinergic pathways leading to symapthoexcitation and hypertension, which can be prevented by blockade of central AT1Rs.50 Sustained activation of these pathways depends on slow neuromodulation in which ENaCs of the ependyma lining the cerebroventricular compartment are activated by binding of aldosterone to central mineralocorticoid receptors. This evidence concerns the gene NR3C2 and hypertensive disorder.