Objective To determine the effects of dexmedetomidine on renal ischemia reperfusion injury (IRI)in rats and to study the underlying mechanisms. Methods Forty SD rats were allocated randomly into 5 groups (n=8 per group). Sham group (S): rats received continuous intravenous infusion of normal saline and clamping the right renal pedicles.IR group (IR): the rats received continuous intravenous infusion of normal saline, and renal IRI was induced by clamping the both renal pedicles 1 h followed by declamping (reperfusion) for 4h. Dex group: intravenous dexmedetomidine was infused continuously at 5 μg/(kg·h)for 1h before the renal ischemia. Dex+Yoh group: yohimbine hydrochloride (1 mg/kg) was administered intravenously 10 min before dexmedetomidine. Yoh group: only yohimbine hydrochloride (1 mg/kg) was administered intravenously 10 min before the renal ischemia. Serum blood urea nitrogen (BUN), creatinine (Cr), kidney superoxide dismutase (SOD) and malonaldehyde (MDA) were detected. Renal histopathology lesions were examined. Results Compared with group S, the serum BUN and Cr, renal MDA inreased while SOD decreased significantly in group IR (P<0.05). Compared with group IR, the serum BUN and Cr, renal MDA decreased while SOD increased significantly in group Dex (P<0.05). The serum BUN and Cr, renal MDA and SOD did not differred in group Dex+Yoh and Yoh (P>0.05). Compared with group S, the pathological scale in group IR, Dex+Yoh and Yoh were higher (P<0.05). The pathological scale in group Dex was lower than that in group IR (P<0.05). Conclusions Dexmedetomidine attenuates renal IRI, partly through the inhibition of oxygen derived free radicals via the activation of the α₂-adrenoceptor.