Aim To investigate the role of reninangiotensin system (RAS) in the cause of fibrinolytic dysfunction. Methods 28 male Wistar rats were randomly divided into four groups: LNNA group: Wistar rats wre administered by intraperinoneol injection of LNNA (15 mg/kg everyday) to induce hypertensive model for 5 weeks; Losartan group and Enalapril group: the hypertensvie model were induced as LNNA group, and treated with losartan (10 mg/kg everyday) or enalapril (10 mg/kg everyday) by gavage from second to fifth week; 4) Control group: treated with normal saline and tap water instead of LNNA and losartan or enalapril in the same procedure. The activity changes of PAI1 and tPA both in plasma and in isolated vessls incubation were mearsured by spectrophotometric assay. Results Significant fibrinolytic dysfunction was found in the LNNA rats, and this dysfunction was markedly improved by the treatment with losartan or enalapril; Compared with the control group, the ability of PAI1 release in isolated vessels of LNNA rats was significantly increased (P<0.01). In the losartan and enalapriltreated group, the baseline levels and thrombininduced release of PAI1 in isolated vessels were reduced by 19%46% and 25%50% respectively (P<0.05), and there is no statistical difference between the two treatment groups. When induced by 10.0 kIU/L thrombin, the tPA release in isolated vessels of LNNA rats were 32% lower than that of controls (P<0.05), and this decline was not improved by the treatment with losartan and enalapril. Conclusions The regulation of RAS on fibrinolysis system is to accelerate the release of PAI1, which is mediated by Angiotensin Ⅱ.