Abstract: Objective To investigate the effects of chronic intermittent hypobaric hypoxia（CIHH）on the vasodilatation of isolated renal artery and the underlying mechanism in rats. Methods Forty-eight adult male SpragueDawley rats were randomly divided into two groups:control group（n=24）and CIHH group（n=24）. The rats in the CIHH group were exposed to hypobaric hypoxia simulating 5000 mhigh altitude（barometric pressure:404mm Hg,oxygen partial pressure:84mm Hg）for 28 days,with 6 hours each day. The rats in the control group were raised in the normoxic environment in the corresponding period. The vasodilatation of renal artery was recorded by isolated vessel ring perfusion method. The protein expression levels of endothelial nitric oxide synthase（eNOS）and phosphoinositide 3kinase（PI3K）in renal artery tissues were determined by Western blot. Results Compared to the control group,the treatment with CIHH could remarkably enhance acetylcholine（ACh）-induced vasodilatation of renal arteryAch(10^-7.5 mol/L):（23.52±3.57）% vs（13.45±2.46）%（n=8）,P＜0.05;Ach(10^-5 mol/L):（78.72±6.13）% vs（49.53±6.64）%（n=8）,P＜0.05;and the treatment with CIHH could increase the expression of eNOS and the concentration of nitric oxide（675.29±56.67）vs（397.17±43.66）μmol/g（n=10）,P＜0.05in the renal artery tissues. The treatment with CIHH could improve the expression of PI3 Kin the renal artery tissues（P＜0.05）. PI3 Kinhibitor LY294002could block the vasodilatation of renal artery and the increase in the expression of eNOS caused by CIHH（P＜0.05）. Conclusion The treatment with CIHH enhances ACh-induced vasodilatation of renal artery possibly by activating eNOS via PI3 Kpathway.