['Renal ischemia reperfusion (IR) injury has been a major source of concern during the past decades and angiotensin converting enzyme (ACE) inhibitors have been successfully used to prevent this injury. There have been some controversial reports about the involvement of K(ATP) channels in the mechanism of action of ACE inhibitors. In this study, we examined the effect of K(ATP) channel blocker (Glibenclamide) on preventive effect of captopril on renal IR injury.', 'Male sprauge-dawley rats were pretreated with glibenclamide (1, 5 and 25 mg/kg) and/or captopril (5 mg/kg). They were anesthetized using ketamine (50 mg/kg) and xylazine (10 mg/kg). The left flank was incised and the left renal artery was clamped for 30 minutes. After that, the kidney was reperfused for 2 hours and then the animal was killed. The Right and left kidneys were removed and evaluated for microscopic damage.', 'Captopril reduced renal IR injury while glibenclamide by itself caused no change. Glibenclamide did not change the preventive effect of captopril.'] Is the mechanism of preventive effect of captopril on renal ischemia reperfusion injury independent of ATP dependent potassium channels?