Aim To observe the affection of angiotensin Ⅱ（AngⅡ） on hypoxia-inducible factor-1（HIF-1α）, vascular endothelial growth factor （VEGF）, prolyl hydroxylases-2 （PHD2）, factor inhibiting hypoxia-inducible factor-1（FIH-1）, and p-ERK expression in human umbilical artery smooth muscle cells （HUASMC）, and clarify the mechanism of PHD2, FIH-1, and p-ERK on HIF-1α expression on the condition of AngⅡ. Method HUASMC were divided into: （1） Control group: normal culture medium for 6 hours （2） AngⅡ group: 10^－6 mol/L AngⅡ culture medium for 6 hours （3） AngⅡ+PD98059 group: 10^－5 mol/L PD98059 added 1 hour before 10^－6 mol/L AngⅡ, and then for 6 hours.Gene expression of HIF-1α, VEGF, PHD2 and FIH-1 were checked by real-time PCR, and the corresponding proteins of above factors, and the p-ERK activation were checked with Western blot. Results （1） Compared with control group, AngⅡ promoted both gene and protein expression of HIF-1α and VEGF （P＜0.05）, and activated p-ERK （P＜0.05）, with the decreased FIH-1 gene and protein expression （P＜0.05）, but has no effect on PHD2 gene and protein expression in HUASMC. （2） Compared with AngⅡ group, both gene and protein expression of HIF-1α, VEGF and the p-ERK activation were significantly reduced （P＜0.05）, with the increased gene and protein expression of FIH-1（P＜0.05） in HUASMC. Conclusions （1） AngⅡ promoted both gene and protein expression of HIF-1α and VEGF in HUASMC.Its mechanism is that activated ERK pathway inhibited FIH-1, leading post-translational reduction of degradation of HIF-1α. （2） ERK inhibitor weakened the promoted affection of AngⅡ on HIF-1α and VEGF.