The antihypertensive therapy with blocked of renin isolated or associate to others drugs is still underexplored in two-kidney one-clip hypertension (2K1C). We investigate the aorta vascular reactivity with aliskiren and its association with L-arginine. Seven days after renal artery clipped, male rats (140-160g, n=8) was divided: 2K1C, 2K1C treated with aliskiren (ALSK) (50 mg/kg /day for 21 days) and 2K1C treated with aliskiren+ L-arginine (L-arg+ALSK). After treatments, rats were anesthetized with pentobarbital (35 mg/kg,i.p.) and killed by exsanguination. The vascular reactivity was analyzed by concentration-response curves to phenylephrine (phen,1 nM-100 µM) and acetylcholine (ach,0.1 nM-300 µM). Were performed blocks (N (G)-nitro-L-argininemethy Ester – L-NAME (100 µM), losartan (10 µM),enalapril (10 µM), incubation with superoxide dismutase(SOD,150 U/ml) and apocynin (0.3 µM). Systolic blood pressure (SBP) was measure before and after treatments by plethysmography and was weighing the left ventricle (LV). In addition, we evaluated the expression of endothelial nitric oxide synthase (eNOS) by the method of Western blotting. Values are means ± S.E.M., compared by ANOVA. (CEUA: 04/2010).The treatments had the following effects: SBP reduced only in the group ALSK + L-Arg (138 ± 4.3 mmHg, P<0.05) compared 2K1C and ALSK groups (204 ± 12.7 and 202 ± 17.7 mmHg, respectively). Was demonstrated that treatment L-arg + ALSK was able to reduce ventricular hypertrophy promoted by hypertension (2K1C:3.32±0.17 mg/g ALSK:2.74±0.14 mg/g ALSK+L- arg:2.58±0.26 mg, P<0.05). 2K1C showed an increase in the concentration response curve to phen and in ALSK and ALSK+L- arg groups this response was reduce. The vasodilator response to ach showed a loss in 2K1C group compared to group ALSK+L-arg. The endothelium removal or incubation with L-NAME increased the vasoconstrictor response to phen in all groups. Apocynin was able to reduce the constrictor response to phen in 2K1C and ALSK+L-arg, however showed no differences in group ALSK. Incubation with SOD showed a decrease in the contractile response to phen in the 2K1C, but no difference in the treated groups. Losartan decrease in contraction to phen in 2K1C and ALSK + L-arg, but not in ALSK group and Enalapril reduce the contractile response only in 2K1C group. In aortic tissue the 2K1C group showed an increase in eNOS protein expression when compared to treatments. The 2K1C showed increase in vascular reactivity to phen, impaired relaxation to acetylcholine and increased expression of eNOS, which seems to be a compensatory mechanism. The ALSK decreased the hyperactivity to phen and expression of eNOS. ALSK+L-arg reduced SBP, vascular reactivity, LV hypertrophy and eNOS expression.These data suggest an important modulation of the renin-angiotensin system and reactive oxygen species in aorta of renovascular hypertension.