Although sensitivity to high dietary NaCl is regarded to be a risk factor for cardiovascular disease, the causes of salt-sensitive hypertension remain elusive. Previously we have shown that rats pretreated with sub-pressor doses of either angiotensin II (ANG II) or aldosterone (Aldo) show sensitized hypertensive responses to a mildly pressor dose of ANG II when tested after an intervening delay. The current studies investigated whether such treatments will induce salt-sensitivity. In studies employing an Induction-Delay-Expression experimental design, male rats were instrumented for chronic blood pressure (BP) recording. In separate experiments, ANG II, Aldo or vehicle were delivered either subcutaneously or intracerebroventricularly during Induction. There were no sustained differences in BP during Delay prior to being given 2% saline. While consuming 2% saline during Expression, both ANG II- and Aldo-pretreated rats showed significantly greater hypertension. When hexamethonium was used to assess autonomic control of BP, no differences in the decrease of BP in response ganglionic blockade were detected during Induction. However, during Expression the fall was greater in sensitized rats. In separate experiments, brain tissue collected at the end of Delay showed increases in message or activation of putative markers of neuroplasticity (i.e., brain-derived neurotrophic factor, p38 mitogen-activated protein kinase, cAMP response element-binding protein). These experiments demonstrate that prior administration of non-pressor doses of either ANG II or Aldo will induce salt-sensitivity. Collectively our findings indicate that treatment with sub-pressor doses of ANG II and Aldo initiate central neuroplastic changes that are involved in hypertension of different etiologies.