Abstract：【Objective】The purpose of this study was to investigate the effect of brain natriuretic peptide（BNP）on mice of heart failure induced by pressure overload in vivo and to clarify the mechanism underlying this effect.【Methods】 C57/B6J mice were transfected with adeno-associated virus（serotype 9，AAV9）encoding the human BNP（hBNP） gene，and the mice of heart failure induced by pressure overload were generated by 3 weeks of aortic banding. After 4 weeks of aortic banding，echocardiography，the ratios of heart weight/body weight（HW/BW） and lung weight/body weight（LW/BW）were used to evaluate the changes of cardiac function and structure，and the mRNA expression level of cardiac hypertrophic marker（ANP） was detected by Q- PCR. The changes of cardiac capillaries were observed by immunofluorescence staining，and the ratio of capillary/myocyte and capillaries density were determined by Image- J software. The mRNA and protein expression of cardiac angiogenesis factors（VEGFA，AngⅠ）were examined by Q-PCR and Western blotting.【Result】Our data showed that AVV9-hBNP notably promoted overexpression of hBNP in mice. Treatment with hBNP not only significantly improved heart failure induced by pressure overload（P < 0.05），but also decreased the ratios of HW/BW and LW/BW as well as the mRNA expression level of hypertrophic marker（P < 0.05）Furthermore，Treatment with hBNP increased cardiac angiogenesis and the mRNA and protein expression level of angiogenesis factors in mice of heart failure （P < 0.05）. 【Conclusion】Treatment with BNP can improve pressure overload-induced heart failure by regulating angiogenesis through promoting the expression of angiogenesis factors.