Acute renal failure following hemorrhagic shock was studied in awake rats. The animals were bled to maintain the mean arterial blood pressure between 40 and 60 mm Hg during 180 min. After this period, the blood was reinfused and the rats were studied 24 h later. Hemorrhagic shock caused a less intensive renal injury than 60-min bilateral renal artery clamping. Renal function in the latter model was worse (p<0.05) as shown by serum creatinine (SCr) (0.75±0.10 vs 1.2±0.2 mg/dL), blood urea nitrogen (BUN) (26.0±2.8 vs 53.0±8.5 mg/dL), fractional excretion of sodium (FENa'%) (0.3±0.1 vs 1.8±1.0) and potassium (FEK'%) (41.4±5.7 vs 76.3±14.2) and urine/plasma creatine (U/PCr(86.4±15.7 vs 38.8±15.5). The rats which received verapamil (10μg/kg/min) prior and during the HS did not show increase in SCr(0.5±0.06 vs 0.75±0.1 mg/dL, p<0.05). This effect was also observed in the rats which received intravenous allopurinol (40 mg/kg) before HS, SCrdid not increase (0.5±0.04 vs 0.75±0.1 mg/dL, p = 0.05), suggesting a protective effect of those substances in HS. Otherwise, when higher doses (50 mg/kg) of allopurinol were injected intra-arterially before and after the HS there was marked worsening of the renal function (p<0.05), measured by SCr(1.5±0.3 vs 0.75±0.1 mg/dL), BUN (117.0±6.9vs 26.6±2.8 mg/dL), FENa(2.1±0.7 vs 0.3±0.1%), FEK(91.0±4.3% vs 41.4±5.7) and U/PCr(16.5±2.2 vs 86.4±15.7). The rats subjected to previous dehydration and pretreatment with gentamicin did not show worsening of renal function when subjected to HS. In conclusion, it was observed that 180-min HS in awake rats is a less intensive insult than 60-min bilateral renal artery clamping. The protective effect of verapamil and allopurinol in HS suggests the participation of cytosolic calcium and oxygen free radicals. However, higher doses of allopurinol given intra-arterially might cause ARF, instead of protecting against ischemia. Dehydration and pretreatment with gentamicin did not aggravate renal ischemia of the hemorrhagic shock.