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Wieslawa Maniara - One of the best experts on this subject based on the ideXlab platform.
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effects of Aliskiren on blood pressure albuminuria and pro renin receptor expression in diabetic tg mren 2 27 rats
Hypertension, 2008Co-Authors: David Louis Feldman, Liang Jin, Hong Xuan, Aurelie Contrepas, Yinong Zhou, Randy Lee Webb, Dominik N Mueller, Sandra Feldt, Frederick Cumin, Wieslawa ManiaraAbstract:The aim of this study was to explore the effects of the renin inhibitor Aliskiren in streptozotocin-diabetic TG(mRen-2)27 rats. Furthermore, we investigated in vitro the effect of Aliskiren on the interactions between renin and the (pro)renin receptor and between Aliskiren and prorenin. Aliskiren distributed extensively to the kidneys of normotensive (non)diabetic rats, localizing in the glomeruli and vessel walls after 2 hours exposure. In diabetic TG(mRen-2)27 rats, Aliskiren (10 or 30 mg/kg per day, 10 weeks) lowered blood pressure, prevented albuminuria, and suppressed renal transforming growth factor-beta and collagen I expression versus vehicle. Aliskiren reduced (pro)renin receptor expression in glomeruli, tubules, and cortical vessels compared to vehicle (in situ hybridization). In human mesangial cells, Aliskiren (0.1 micromol/L to 10 micromol/L) did not inhibit binding of (125)I-renin to the (pro)renin receptor, nor did it alter the activation of extracellular signal-regulated kinase 1/2 by renin (20 nmol/L) preincubated with Aliskiren (100 nmol/L) or affect gene expression of the (pro)renin receptor. Evidence was obtained that Aliskiren binds to the active site of prorenin. The above results demonstrate the antihypertensive and renoprotective effects of Aliskiren in experimental diabetic nephropathy. The evidence that Aliskiren can reduce in vivo gene expression for the (pro)renin receptor and that it may block prorenin-induced angiotensin generation supports the need for additional work to reveal the mechanism of the observed renoprotection by this renin inhibitor.
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effects of Aliskiren on blood pressure albuminuria and pro renin receptor expression in diabetic tg mren 2 27 rats
Hypertension, 2008Co-Authors: David Louis Feldman, Liang Jin, Hong Xuan, Aurelie Contrepas, Yinong Zhou, Randy Lee Webb, Dominik N Mueller, Sandra Feldt, Frederick Cumin, Wieslawa ManiaraAbstract:The aim of this study was to explore the effects of the renin inhibitor Aliskiren in streptozotocin-diabetic TG(mRen-2)27 rats. Furthermore, we investigated in vitro the effect of Aliskiren on the interactions between renin and the (pro)renin receptor and between Aliskiren and prorenin. Aliskiren distributed extensively to the kidneys of normotensive (non)diabetic rats, localizing in the glomeruli and vessel walls after 2 hours exposure. In diabetic TG(mRen-2)27 rats, Aliskiren (10 or 30 mg/kg per day, 10 weeks) lowered blood pressure, prevented albuminuria, and suppressed renal transforming growth factor-β and collagen I expression versus vehicle. Aliskiren reduced (pro)renin receptor expression in glomeruli, tubules, and cortical vessels compared to vehicle (in situ hybridization). In human mesangial cells, Aliskiren (0.1 μmol/L to 10 μmol/L) did not inhibit binding of 125 I-renin to the (pro)renin receptor, nor did it alter the activation of extracellular signal-regulated kinase 1/2 by renin (20 nmol/L) preincubated with Aliskiren (100 nmol/L) or affect gene expression of the (pro)renin receptor. Evidence was obtained that Aliskiren binds to the active site of prorenin. The above results demonstrate the antihypertensive and renoprotective effects of Aliskiren in experimental diabetic nephropathy. The evidence that Aliskiren can reduce in vivo gene expression for the (pro)renin receptor and that it may block prorenin-induced angiotensin generation supports the need for additional work to reveal the mechanism of the observed renoprotection by this renin inhibitor.
Randy Lee Webb - One of the best experts on this subject based on the ideXlab platform.
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effects of Aliskiren on blood pressure albuminuria and pro renin receptor expression in diabetic tg mren 2 27 rats
Hypertension, 2008Co-Authors: David Louis Feldman, Liang Jin, Hong Xuan, Aurelie Contrepas, Yinong Zhou, Randy Lee Webb, Dominik N Mueller, Sandra Feldt, Frederick Cumin, Wieslawa ManiaraAbstract:The aim of this study was to explore the effects of the renin inhibitor Aliskiren in streptozotocin-diabetic TG(mRen-2)27 rats. Furthermore, we investigated in vitro the effect of Aliskiren on the interactions between renin and the (pro)renin receptor and between Aliskiren and prorenin. Aliskiren distributed extensively to the kidneys of normotensive (non)diabetic rats, localizing in the glomeruli and vessel walls after 2 hours exposure. In diabetic TG(mRen-2)27 rats, Aliskiren (10 or 30 mg/kg per day, 10 weeks) lowered blood pressure, prevented albuminuria, and suppressed renal transforming growth factor-beta and collagen I expression versus vehicle. Aliskiren reduced (pro)renin receptor expression in glomeruli, tubules, and cortical vessels compared to vehicle (in situ hybridization). In human mesangial cells, Aliskiren (0.1 micromol/L to 10 micromol/L) did not inhibit binding of (125)I-renin to the (pro)renin receptor, nor did it alter the activation of extracellular signal-regulated kinase 1/2 by renin (20 nmol/L) preincubated with Aliskiren (100 nmol/L) or affect gene expression of the (pro)renin receptor. Evidence was obtained that Aliskiren binds to the active site of prorenin. The above results demonstrate the antihypertensive and renoprotective effects of Aliskiren in experimental diabetic nephropathy. The evidence that Aliskiren can reduce in vivo gene expression for the (pro)renin receptor and that it may block prorenin-induced angiotensin generation supports the need for additional work to reveal the mechanism of the observed renoprotection by this renin inhibitor.
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effects of Aliskiren on blood pressure albuminuria and pro renin receptor expression in diabetic tg mren 2 27 rats
Hypertension, 2008Co-Authors: David Louis Feldman, Liang Jin, Hong Xuan, Aurelie Contrepas, Yinong Zhou, Randy Lee Webb, Dominik N Mueller, Sandra Feldt, Frederick Cumin, Wieslawa ManiaraAbstract:The aim of this study was to explore the effects of the renin inhibitor Aliskiren in streptozotocin-diabetic TG(mRen-2)27 rats. Furthermore, we investigated in vitro the effect of Aliskiren on the interactions between renin and the (pro)renin receptor and between Aliskiren and prorenin. Aliskiren distributed extensively to the kidneys of normotensive (non)diabetic rats, localizing in the glomeruli and vessel walls after 2 hours exposure. In diabetic TG(mRen-2)27 rats, Aliskiren (10 or 30 mg/kg per day, 10 weeks) lowered blood pressure, prevented albuminuria, and suppressed renal transforming growth factor-β and collagen I expression versus vehicle. Aliskiren reduced (pro)renin receptor expression in glomeruli, tubules, and cortical vessels compared to vehicle (in situ hybridization). In human mesangial cells, Aliskiren (0.1 μmol/L to 10 μmol/L) did not inhibit binding of 125 I-renin to the (pro)renin receptor, nor did it alter the activation of extracellular signal-regulated kinase 1/2 by renin (20 nmol/L) preincubated with Aliskiren (100 nmol/L) or affect gene expression of the (pro)renin receptor. Evidence was obtained that Aliskiren binds to the active site of prorenin. The above results demonstrate the antihypertensive and renoprotective effects of Aliskiren in experimental diabetic nephropathy. The evidence that Aliskiren can reduce in vivo gene expression for the (pro)renin receptor and that it may block prorenin-induced angiotensin generation supports the need for additional work to reveal the mechanism of the observed renoprotection by this renin inhibitor.
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Aliskiren a novel orally effective renin inhibitor lowers blood pressure in marmosets and spontaneously hypertensive rats
Journal of Hypertension, 2005Co-Authors: Jeanette Marjorie Wood, Christian Schnell, Frederic Cumin, Joel Menard, Randy Lee WebbAbstract:Objectives Aliskiren is a new renin inhibitor of a novel structural class that has recently been shown to be efficacious in hypertensive patients after once-daily oral dosing. We report the results of animal experiments performed in marmosets and rats in order to characterize Aliskiren before its recent investigation in humans. Methods The effects of Aliskiren were investigated in sodium-depleted marmosets (oral dosing) and in spontaneously hypertensive rats (dosing via subcutaneous osmotic minipumps). Blood pressure (BP) and heart rate were measured by radiotelemetry. Results In sodium-depleted marmosets, single oral doses of Aliskiren (1-30 mg/kg) dose-dependently lowered BP. At a dose of 3 mg/kg, peak effects were observed 1 h after dosing (−30 ± 4 mmHg, n = 6) and the response persisted for more than 12 h. A single oral dose of 3 mg/kg Aliskiren was more effective than the same dose of either remikiren or zankiren, two orally active renin inhibitors previously tested in humans. Aliskiren (10 mg/kg) was at least as effective as equal doses of the AT1-receptor blocker valsartan or the angiotensin-converting enzyme inhibitor benazepril. In spontaneously hypertensive rats, Aliskiren dose-dependently (10-100 mg/kg per day) decreased BP. Aliskiren also potentiated the antihypertensive effects of low doses of valsartan or benazeprilat (1 or 3 mg/kg per day). Conclusions Aliskiren is an orally effective, long-lasting renin inhibitor that shows antihypertensive efficacy in animals superior to previous renin inhibitors and at least equivalent to angiotensin-converting enzyme inhibitors and AT1-receptor blockers. Aliskiren may therefore represent an effective, novel approach to the treatment of hypertension and related disorders, alone or in combination with other antihypertensive agents.
Deborah L Keefe - One of the best experts on this subject based on the ideXlab platform.
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safety and tolerability of the direct renin inhibitor Aliskiren in combination with angiotensin receptor blockers and thiazide diuretics a pooled analysis of clinical experience of 12 942 patients
Journal of Clinical Hypertension, 2011Co-Authors: William B White, Robert S Bresalier, Allen P Kaplan, Biff F Palmer, Robert H Riddell, Anastasia Lesogor, William Chang, Deborah L KeefeAbstract:Combinations of the direct renin inhibitor Aliskiren with angiotensin receptor blockers (ARBs) or diuretics are effective therapeutic regimens for the treatment of hypertension. A large database of safety information has become available during the past several years with Aliskiren in combination trials. Data were pooled from 9 short-term (8-week) and 4 longer-term (26- to 52-week) randomized controlled trials of Aliskiren in patients with hypertension. Adverse event (AE) rates were assessed for Aliskiren combination therapy compared with component monotherapies. In short-term studies, overall AE rates were similar for patients receiving Aliskiren/valsartan or Aliskiren/diuretic combinations (32.2%-39.8%) and those receiving the component monotherapies (30.0%-39.6%). In longer-term studies, AE rates with Aliskiren/losartan (55.5%) and Aliskiren/diuretic (45.0%) combination therapy were similar to those with losartan (53.9%) and diuretic (48.9%) alone. Angioedema and hyperkalemia occurred in similar proportions of patients taking combination therapies vs monotherapy. The safety and tolerability profile of Aliskiren in combination with the ARBs valsartan or losartan, or diuretic, is similar to Aliskiren, ARBs, or diuretics alone.
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safety and tolerability of the direct renin inhibitor Aliskiren a pooled analysis of clinical experience in more than 12 000 patients with hypertension
Journal of Clinical Hypertension, 2010Co-Authors: William B White, Robert S Bresalier, Allen P Kaplan, Biff F Palmer, Robert H Riddell, Anastasia Lesogor, William Chang, Deborah L KeefeAbstract:While the safety of renin-angiotensin system (RAS)-blocking drugs such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers is well known, less is known about the new direct renin inhibitor Aliskiren. The authors pooled data from 12 randomized controlled trials of Aliskiren in patients with hypertension and analyzed the incidence and types of adverse events (AEs) and laboratory abnormalities. Studies were characterized as short-term (≤2 months) placebo-controlled or long-term (>2 months) active-controlled. Relative risks for AEs of particular interest for RAS blockers were calculated. In short-term studies, AEs occurred in similar proportions of Aliskiren 150 mg and 300 mg (33.6% and 31.6%, respectively) and placebo treatment groups (36.8%). In long-term studies, a lower proportion of patients treated with Aliskiren 150 mg and 300 mg had AEs (33.7% and 43.2%, respectively) than those treated with ACE inhibitors (60.1%), angiotensin receptor blockers (53.9%), and thiazide diuretics (48.9%). Events of special interest, including angioedema, hyperkalemia, and diarrhea occurred in similar proportions of patients taking Aliskiren, placebo, and comparator agents. In studies of up to 36 weeks, patients treated with Aliskiren were significantly less likely to develop cough than those treated with ACE inhibitors. At the registered doses of 150 mg and 300 mg daily, Aliskiren has safety and tolerability profiles similar to placebo, other RAS blockers, and diuretics. Cough rates are lower with Aliskiren compared with ACE inhibitors.
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Aliskiren for geriatric lowering of systolic hypertension a randomized controlled trial
Journal of Human Hypertension, 2010Co-Authors: Daniel Duprez, Deborah L Keefe, M A Munger, Jaco Botha, A N CharneyAbstract:Efficacy and safety of the direct renin inhibitor Aliskiren was compared with ramipril for treatment of essential systolic hypertension in elderly patients. A 36-week, randomized, double-blind, parallel-group, active-controlled, optional-titration study was performed in 901 patients (Aliskiren, n=457; ramipril, n=444) > or =65 years of age with systolic blood pressure (SBP) > or =140 mm Hg. Aliskiren 150-300 mg per day or ramipril 5-10 mg per day for was administered for 12 weeks with optional add-on therapy of hydrochlorothiazide (12.5-25 mg per day) at week 12 and amlodipine (5-10 mg per day) at week 22. The primary end point was non-inferiority of Aliskiren vs ramipril monotherapy for change from baseline in mean sitting SBP (msSBP) at week 12. Decreases from baseline msSBP and mean sitting diastolic BP with Aliskiren monotherapy (-14.0 and -5.1 mm Hg, respectively) were non-inferior (P<0.001 for both values) and superior to ramipril monotherapy (-11.6, -3.6 mm Hg; P=0.02, P<0.01, respectively). More patients achieved BP control with Aliskiren (42%) than ramipril (33%; P<0.01). At week 36, fewer patients receiving Aliskiren-based therapy required add-on treatment with hydrochlorothiazide or amlodipine (P=0.01 and 0.048, respectively). Tolerability was similar, but more patients receiving ramipril reported cough (P<0.001). In elderly patients with systolic hypertension, Aliskiren proved to be more effective and better overall anti-hypertensive therapy compared to ramipril.
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Influence of body weight and gender on the pharmacokinetics, pharmacodynamics, and antihypertensive efficacy of Aliskiren.
Journal of clinical pharmacology, 2010Co-Authors: Venkateswar Jarugula, Deborah L Keefe, Dan Howard, Ching Ming Yeh, Christopher Bush, William P. DoleAbstract:Gender and body weight influence the pharmacokinetics and pharmacodynamics of many drugs. This pooled analysis of 17 clinical studies evaluated the effect of gender, body mass index (BMI), body weight, and lean body weight (LBW) on the pharmacokinetics of the direct renin inhibitor Aliskiren in healthy volunteers (n = 392). A separate pooled analysis of 5 clinical studies in patients with hypertension (n = 2327) assessed the influence of gender and BMI on the effects of Aliskiren on plasma renin activity and blood pressure. Area under the Aliskiren plasma concentration-time curve (AUC(τ)) was 22% lower and the peak Aliskiren plasma concentration (C(max)) was 24% lower in men than women (P < .05). BMI was not significantly correlated with AUC(τ) (r = 0.005; P = .917); AUC(τ) was negatively correlated with body weight (r = -0.235; P < .0001) and LBW (r = -0.295; P < .0001). Results were similar for C(max). Adjusting individual Aliskiren AUC(τ) and C(max) values for overall mean body weight or LBW abolished gender differences. Based on r(2) values, LBW variation accounted for 8.9% of Aliskiren AUC(τ) variation. In patients with hypertension, gender and BMI did not significantly influence the effects of Aliskiren on plasma renin activity or blood pressure. It was concluded that lower systemic exposure to Aliskiren in men versus women relates to differences in body weight; neither gender nor body weight has clinically relevant effects on the pharmacokinetics or pharmacodynamics of Aliskiren.
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comparative effects of Aliskiren based and ramipril based therapy on the renin system during long term 6 months treatment and withdrawal in patients with hypertension
Journal of the Renin-Angiotensin-Aldosterone System, 2009Co-Authors: Karl Andersen, Myron H Weinberger, Christian M Constance, Mohammed Atif Ali, James Jin, Margaret F Prescott, Deborah L KeefeAbstract:Introduction. This subgroup analysis assessed the effects of treatment based on the direct renin inhibitor, Aliskiren, or the angiotensin- converting enzyme inhibitor, ramipril, on plasma renin activity (PRA), plasma renin concentration (PRC) and other biomarkers in a 26-week randomised, double-blind trial. Changes in PRA and PRC after stopping treatment were also assessed. Methods. After placebo run-in, 842 patients (mean sitting diastolic blood pressure (BP) 95-109 mmHg) were randomised to Aliskiren 150 mg or ramipril 5 mg. Dose titration and hydrochlorothiazide addition were allowed after Week 6 and 12, respectively, for inadequate BP control. Patients completing active treatment were re-randomised to current regimen or placebo during a 4-week post- treatment phase. Results. BP reductions were independent of baseline PRA at Week 12, were greater with Aliskiren- than ramipril-based therapy at Week 26 (17.9/13.3 vs. 15.2/12.0 mmHg, p<0.05) and persisted for longer after stopping Aliskiren. Aliskiren-based therapy reduced geometric mean PRA (−63%, p<0.05; n=103), while ramipril-based therapy increased PRA (+143%, p<0.05; n=100) at Week 26; PRC increased in both groups (Aliskiren: +224% (n=33), ramipril: +145% (n=39), both p<0.05). Four weeks after stopping Aliskiren-based therapy, PRA remained 52% below pre-treatment baseline; PRA returned to baseline 2 weeks after stopping ramipril- based therapy. Conclusions. Aliskiren-based therapy produced sustained BP and PRA reductions over 26 weeks; ramipril-based therapy lowered BP and increased PRA. PRA reductions persisted 4 weeks after stopping Aliskiren, suggesting an inhibitory effect beyond the elimination half-life of the drug.
David Louis Feldman - One of the best experts on this subject based on the ideXlab platform.
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effects of Aliskiren on blood pressure albuminuria and pro renin receptor expression in diabetic tg mren 2 27 rats
Hypertension, 2008Co-Authors: David Louis Feldman, Liang Jin, Hong Xuan, Aurelie Contrepas, Yinong Zhou, Randy Lee Webb, Dominik N Mueller, Sandra Feldt, Frederick Cumin, Wieslawa ManiaraAbstract:The aim of this study was to explore the effects of the renin inhibitor Aliskiren in streptozotocin-diabetic TG(mRen-2)27 rats. Furthermore, we investigated in vitro the effect of Aliskiren on the interactions between renin and the (pro)renin receptor and between Aliskiren and prorenin. Aliskiren distributed extensively to the kidneys of normotensive (non)diabetic rats, localizing in the glomeruli and vessel walls after 2 hours exposure. In diabetic TG(mRen-2)27 rats, Aliskiren (10 or 30 mg/kg per day, 10 weeks) lowered blood pressure, prevented albuminuria, and suppressed renal transforming growth factor-beta and collagen I expression versus vehicle. Aliskiren reduced (pro)renin receptor expression in glomeruli, tubules, and cortical vessels compared to vehicle (in situ hybridization). In human mesangial cells, Aliskiren (0.1 micromol/L to 10 micromol/L) did not inhibit binding of (125)I-renin to the (pro)renin receptor, nor did it alter the activation of extracellular signal-regulated kinase 1/2 by renin (20 nmol/L) preincubated with Aliskiren (100 nmol/L) or affect gene expression of the (pro)renin receptor. Evidence was obtained that Aliskiren binds to the active site of prorenin. The above results demonstrate the antihypertensive and renoprotective effects of Aliskiren in experimental diabetic nephropathy. The evidence that Aliskiren can reduce in vivo gene expression for the (pro)renin receptor and that it may block prorenin-induced angiotensin generation supports the need for additional work to reveal the mechanism of the observed renoprotection by this renin inhibitor.
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effects of Aliskiren on blood pressure albuminuria and pro renin receptor expression in diabetic tg mren 2 27 rats
Hypertension, 2008Co-Authors: David Louis Feldman, Liang Jin, Hong Xuan, Aurelie Contrepas, Yinong Zhou, Randy Lee Webb, Dominik N Mueller, Sandra Feldt, Frederick Cumin, Wieslawa ManiaraAbstract:The aim of this study was to explore the effects of the renin inhibitor Aliskiren in streptozotocin-diabetic TG(mRen-2)27 rats. Furthermore, we investigated in vitro the effect of Aliskiren on the interactions between renin and the (pro)renin receptor and between Aliskiren and prorenin. Aliskiren distributed extensively to the kidneys of normotensive (non)diabetic rats, localizing in the glomeruli and vessel walls after 2 hours exposure. In diabetic TG(mRen-2)27 rats, Aliskiren (10 or 30 mg/kg per day, 10 weeks) lowered blood pressure, prevented albuminuria, and suppressed renal transforming growth factor-β and collagen I expression versus vehicle. Aliskiren reduced (pro)renin receptor expression in glomeruli, tubules, and cortical vessels compared to vehicle (in situ hybridization). In human mesangial cells, Aliskiren (0.1 μmol/L to 10 μmol/L) did not inhibit binding of 125 I-renin to the (pro)renin receptor, nor did it alter the activation of extracellular signal-regulated kinase 1/2 by renin (20 nmol/L) preincubated with Aliskiren (100 nmol/L) or affect gene expression of the (pro)renin receptor. Evidence was obtained that Aliskiren binds to the active site of prorenin. The above results demonstrate the antihypertensive and renoprotective effects of Aliskiren in experimental diabetic nephropathy. The evidence that Aliskiren can reduce in vivo gene expression for the (pro)renin receptor and that it may block prorenin-induced angiotensin generation supports the need for additional work to reveal the mechanism of the observed renoprotection by this renin inhibitor.
Lin Zhou - One of the best experts on this subject based on the ideXlab platform.
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Protective effects of Aliskiren on ischemia–reperfusion-induced renal injury in rats
European Journal of Pharmacology, 2013Co-Authors: Zhen Wang, Yukai Liu, Yu Han, Weiwei Guan, Xun Kou, Di Yang, Hongmei Ren, Lin ZhouAbstract:The protective effect of Aliskiren on ischemia-reperfusion (I/R) injury in the heart and brain has been reported. Whether or not this protective effect extends into the alleviation of renal I/R injury is not known. Therefore, we investigated the protective effect of Aliskiren in the kidney in this study. Sprague-Dawley rats were randomly divided into four groups: sham control group; sham control with Aliskiren pretreatment; I/R group and I/R with Aliskiren pretreatment. Aliskiren (3mg/kg) or vehicle was administrated intravenously via vena cava. Blood samples and the left kidneys were then collected to check for renal function, angiotensin II (Ang II), apoptosis and oxidative stress levels. Compared with the sham rats, serum creatinine (SCR) and blood urea nitrogen (BUN) were significantly increased in the I/R rats, accompanied by histopathological damage to the kidney, which included tubular cell swelling, desquamation, and cast formation. There were also more apoptotic cells and leukocyte infiltration in the I/R rats than in the sham rats. Pretreatment with Aliskiren ameliorated I/R induced renal injury, i.e. reduced SCR and BUN levels, ameliorated renal histopathological changes, and decreased the apoptosis of cells and leukocyte infiltration in kidney. I/R injury also decreased superoxide dismutase (SOD) and glutathione (GSH-reduced form) levels, which were blocked with the Aliskiren pretreatment. Aliskiren pretreatment exerts a protective effect on ischemia/reperfusion injury in the kidney, via amelioration of oxidative stress, and reduction in leukocyte infiltration and cellular apoptosis.
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Protective effects of Aliskiren on ischemia-reperfusion-induced renal injury in rats.
European journal of pharmacology, 2013Co-Authors: Zhen Wang, Yukai Liu, Yu Han, Weiwei Guan, Xun Kou, Di Yang, Hongmei Ren, Lin ZhouAbstract:The protective effect of Aliskiren on ischemia-reperfusion (I/R) injury in the heart and brain has been reported. Whether or not this protective effect extends into the alleviation of renal I/R injury is not known. Therefore, we investigated the protective effect of Aliskiren in the kidney in this study. Sprague-Dawley rats were randomly divided into four groups: sham control group; sham control with Aliskiren pretreatment; I/R group and I/R with Aliskiren pretreatment. Aliskiren (3mg/kg) or vehicle was administrated intravenously via vena cava. Blood samples and the left kidneys were then collected to check for renal function, angiotensin II (Ang II), apoptosis and oxidative stress levels. Compared with the sham rats, serum creatinine (SCR) and blood urea nitrogen (BUN) were significantly increased in the I/R rats, accompanied by histopathological damage to the kidney, which included tubular cell swelling, desquamation, and cast formation. There were also more apoptotic cells and leukocyte infiltration in the I/R rats than in the sham rats. Pretreatment with Aliskiren ameliorated I/R induced renal injury, i.e. reduced SCR and BUN levels, ameliorated renal histopathological changes, and decreased the apoptosis of cells and leukocyte infiltration in kidney. I/R injury also decreased superoxide dismutase (SOD) and glutathione (GSH-reduced form) levels, which were blocked with the Aliskiren pretreatment. Aliskiren pretreatment exerts a protective effect on ischemia/reperfusion injury in the kidney, via amelioration of oxidative stress, and reduction in leukocyte infiltration and cellular apoptosis.