THE ROLE OF ATP SENSITIVE K+ CHANNELS (KATP) ON ISCHEMIA REPERFUSION INDUCED RENAL INJURY IN RATS

The precise mechanism of ischemia reperfusion (IR) injury is not fully understood. Recent studies on Rat myocardium revealed that activation of the K ATP channels inhibits this process. The goal of this study is finding the same effect of K ATP channels on IR injury, in rat kidney. In this study the effects of K ATP agonist (Diazoxide) and K ATP antagonist (Glibenclamide) plus a K ATP independent vasodilator (Hydralazin) on ischemia reperfusion injury examined. Female rats of 200-250 g were anesthesized and used for study. Different doses of Diazoxide (1, 5, 15mg/kg) and Glibenclamid (1, 5, 10mg/kg) and hydralazin (1, 3, 15mg/kg) were used (SC) 120 minutes prior to the initiation of IR. Kidneys were removed and checked histologically for the grading of injury. Diazoxide (5mg/kg) prevented these lesions. Different doses of Glibenclamide and hydralazine failed to prevent IR injury. Diazoxide is also a vasodilator agent but failure of hydralazine to prevent the injury revealed that vasodilation was not the exact mechanism of action of Diazoxide.