In Dahl salt-sensitive (S) rats, high salt intake increases cerebrospinal fluid (CSF) [Na⁺] and BP. Intra-cerebroventricular (icv) infusion of a mineralocorticoid receptor (MR) blocker prevents the hypertension. To assess the role of aldosterone locally produced in the brain, we evaluated the effects of chronic central blockade with the aldosterone synthase inhibitor FAD286 and the MR blocker spironolactone on changes in aldosterone and corticosterone content in the hypothalamus, and the increase in CSF [Na⁺] and hypertension induced by high salt in Dahl S rats. After 4 weeks on high salt intake, plasma aldosterone and corticosterone were not changed, but hypothalamic aldosterone increased by ~35% and corticosterone tended to increase in Dahl S rats, whereas both steroids decreased by ~65% in Dahl salt-resistant (R) rats. In Dahl S rats on high salt, icv infusion of FAD286 or spironolactone did not affect the increase in CSF [Na⁺]. Icv infusion of FAD286 prevented the increase in hypothalamic aldosterone, and 30 mmHg of the 50 mmHg BP increase induced by high salt. Icv infusion of spironolactone fully prevented the salt-induced hypertension. These results suggest that in Dahl S rats, high salt intake increases aldosterone synthesis in the hypothalamus, and aldosterone acts as the main MR agonist activating central pathways contributing to salt-induced hypertension.