Previous studies suggested that mechanical intervention during early reperfusion, or "ischemia postconditioning" (IPo), could protect kidneys against renal ischemia reperfusion injury (RIRI)[1,2].However, the mechanisms responsible for this protection remain unclear.This study therefore investigated the protection afforded by IPo in rat kidneys in vivo, and the roles of mitochondrial KATe channels (mitoKATe) and mitochondrial permeability transition pores (MPTPs),by inhibiting mitoKATP with 5-hydroxydecanoate (5-HD), and by directly detecting open MPTPs using calcein-AM and CoCl2.