Sympathetic hyperactivity, baroreflex dysfunction and intrarenal alterations are all involved in the renovascular hypertension. It’s already known that most of these changes are mediated by high level of circulating angiotensin II (Ang II) which also releases aldosterone. The aim of this study was to evaluate the effects of spironolactone (Spiro) (200mg/Kg/day) treatment, in a renovascular model of hypertension, the 2 kidney-1 clip (2K-1C). We evaluated in conscious rats changes on mean arterial pressure (MAP) and reflex control of renal sympathetic nerve activity (rSNA) in urethane anaesthetized rats (1.2-1.4 g/Kg). The tonic and reflex control of rSNA was evaluated (1 min infusion of phenylephrine 100 µg/mL/min and sodium nitroprusside 200µg/mL/min). Furthermore, the plasma renin activity (PRA) and the intrarenal renin protein expression; renal fibrosis process (expression of α-actin by imunohistochemistry); type 1 Ang II receptor (AT1) and mineralocorticoid receptor (MR) protein expression in renal tissue and central nervous system (CNS) specifically in regions involved with cardiovascular regulation such as the nucleus of tractus solilaty (NTS) and the rostral ventrolateral medulla (RVLM) were investigated. In 2K-1C group Spiro treatment decreased MAP (2K-1C: 198±4,n=9; 2K-1C+Spiro: 170±9 mmHg,n=8; p<0.05 ANOVA -Tukey) and normalized the rSNA (2K-1C: 147±9,n=6; 2K-1C+Spiro: 96±10 spikes/s,n=8; p<0.05 ANOVA-tukey). Spiro treatment increased rSNA baroreceptor reflex sensitivity in both groups (CT: -0,3±0,04, n=6; CT+Spiro: -0,9±0,03, n=5; 2K-1C: -0,2±0,03, n=5; 2K-1C+Spiro: -0,4±0,03 spikes/s/mmHg, n=5; p<0.05 ANOVA-Tukey). Furthermore, the Spiro treatment decreased expression of α-actin in nonclipped kidneys in 2K-1C group (2K-1C: 5±0,6,n=4; 2K-1C+Spiro: 1,1±0,2, %,n=3; p<0.05 ANOVA- Tukey). There was no changes in PRA in 2K-1C, but a decrease in renin protein expression in nonclippped kidney was found (2K-1C: 217±30, n=5; 2K-1C+Spiro: 160±19, %, n=5; p<0.05 Kruskall Wallis-Dunns). In clipped and nonclipped kidneys of 2K-1C, the AT1 and MR receptors protein expression was not modified by treatment, however, Spiro treatment promoted downregulation of AT1 receptors at the CNS in hypertensive group (RVLM= 2K-1C: 129±10, n=10; 2K-1C+Spiro: 84±12, %, n=5; p<0.05 ANOVA -Tukey; NTS= 2K-1C: 148±29,n=5; 2K-1C+Spiro: 68±14, %, n=4; p=0.06 ANOVA -Tukey). Taken altogether, the results suggest that aldosterone has differential effects in kidneys and CNS. Aldosterone is an important mediator in the tonic and reflex control of rSNA as well as contributes for intrarenal fibrosis process in renovascular hypertension.