【Objective】To determine the effect and molecular mechanisms of aldosterone on the endothelial repaircapacity of endothelial progenitor cells（EPC）in peripheral blood.【Method】EPC were cultured from peripheral blood mononuclear cells of healthy subjects. In vitro EPC function was assayed by migration and adhesion after treatment with different concentration of aldosterone（0，10，100，1000nmol/L）. In vivo endothelial repaircapacity of EPC was evaluated by transplantation into anudemouse carotid endothelial denudation model.The reactive oxygen species（ROS）was detected by 2’， 7’-dichlorodihydro fluoresceindiacetate（DCF）- fluorescen tprobe under fluorescence microscopy.【Result】Both the in vitro function and in vivo endothelial repaircapacity of EPC were impaired obviously by aldosterone treatment. ROS production was distinctly increased after aldosterone treatment as well. Co-treatment with mineralocorticoid receptor inhibitor spironolactone or NADPH oxidase block erapocynin prevented aldosterone-induced ROS production and recovered aldosterone-impaired EPC function.【Conclusion】Aldosterone-induced oxidative stress impairs endothelial repaircapacity of EPC via MR-dependent activation of NADPH oxidase.