It is well known that increase in renal sympathetic nerve activity induces renin release, sodium reabsorption and decrease renal blood flow. However, the exactly mechanism underlying how the sodium reabsorption is processed it is still not well understood. The present study evaluated the effects of renal acute sympathetic nerve electrical stimulation (RSNS) over the gene expression (PCR) of sodium-hydrogen exchanger type 3 (NHE3), epithelial sodium channel (β-ENaC) and water (aquaporin 2 – AQP2) transporters in the kidney in the presence or not of AT1Angiotensin II receptor blockade. Male Wistar rat (250g-300g), were divided in four independent groups: A) Sham (renal sympathetic nerve activity registered for 1h, n=6); B) RSNS for 1h, [15V, 1Hz and 0,5 ms], n=6); C) Sham+Losartan, n=6 (30 mg/kg/day) and D) Losartan+RSNS (n=6). All procedures were performed in anaesthetized animals (sodium tiophental 60mg/Kg, ip). Values are means±SEM compared by ANOVA. Electrical stimulation of renal sympathetic nerve leads to a significant increase in NHE3 (Sham1.0±0.01 vs RSNS 1,6±0,2AU), however, a reduction in β-ENaC (Sham 1,02±,012 vs 0,6±0,1AU) and in AQP2 (Sham 1,06±0,18 vs 0,6±0,1AU) gene expression was found. Animals just treated with Losartan did not present differences at NHE3 expression but a significant reduction of basal renal sympathetic nerve activity was observed (89±4 vs 63±7 pps). Furthermore, a significant reduction in ENAC (0,4±0,1AU) and AQP2 (0,3±0,1UA) expression was induced by losartan when compared to SHAM animals. Treatment with Losartan+RSNS had no effect over the studied transporters. Taken altogether, RSNS produces differential alterations in sodium and water transporters in the renal tubule that can be important for the sodium homeostasis. Apparently, such effects are dependent of AT1 angiotensin II receptor.