Abstract: AIM: To observe the expression of focal adhesion kinase in rat’s autologous vein graft and its modulating effect by olmesartan (a specific type 1 angiotensin II receptor antagonist). METHODS: Autologous external jugular veins were grafted to common carotid arteries in 36 male Wistar rats. After surgery, rats were randomly assigned to three groups (12 rats in each): model control group, olmesartan group and physiological saline group. The intimal thickness in vein grafts was quantitated in H/E-stained segments. Integrin β-3 and focal adhesion kinase expression levels were assessed by Western blotting, and proliferating cell nuclear antigen (PCNA) was measured by immunohistochemistry. RESULTS: Neointimal hyperplasia was observed in model control group characterized by significant intimal thickening. The expressions of integrin β-3, FAK and PCNA were positive in model control group. Compared with that in model control group, the intimal thickness was significantly attenuated in olmesartan group (P<0.05) and the expressions of FAK and PCNA significantly reduced (P<0.05). CONCLUSION: FAK is involved in the restenosis of vein graft in rats. Olmesartan attenuates the restenosis of rat vein graft, possibly through its downregulating effect on FAK.