Abstract: OBJECTIVE To observe the role of Tie-2 in the regulation of angiopoietin-1(Ang-1) and angiopoietin-2(Ang-2) on the biphasic change of vascular reactivity after hemorrhagic shock in rats. METHODS The protein expression and tyrosine phosphorylation of Tie-2 in the superior mesenteric artery(SMA) after hemorrhagic shock were measured via Western blot technique, the effect of Tie-2 inhibitor on the vascular reactivity of SMA in the early (hyperreactivity) and late (hyporeactivity) period of hypoxia treated with Ang-1 and Ang-2 were observed via the isolated organ perfusion system, and the protein expression and tyrosine phosphorylation of Tie-2 in the hypoxia mixture of vascular endothelial cell(VEC) and vascular smooth muscle cell(VSMC) treated with Ang-1 and Ang-2 were measured via Western blot technique. Effect of Tie-2 on the NO concentration of VSMC and VEC mixture in the early and late hypoxia was detected by the NO kit. RESULTS ①The protein expression and tyrosine phosphorylation of Tie-2 in the SMA were low in normal control group, and were increased after hemorrhagic shock, the protein expression of Tie-2 was increased after 30 min shock (P<0.01), and the tyrosine phosphorylation of Tie-2 was increased after 10 min shock (P<0.01), both protein expression and tyrosine phosphorylation of Tie-2 were further increased as shock went on (P<0.01). ②Tie-2 inhibitor could decrease the vascular hyperreactivity in 10 min hypoxia (the Emax of NE was decreased from 13.479 mN to 10.122 mN, P<0.05), and repress the maintenance effect of Ang-1 on vascular reactivity in 10 min hypoxia (the Emax of NE was decreased from 15.283 mN to 10.253 mN, P<0.01); Tie-2 inhibitor could improve the vascular hyporeactivity in 4 h hypoxia (the Emax of NE was increased from 5.875 mN to 8.003 mN, P<0.05), and inhibit the decrease effect of Ang-2 on vascular reactivity in 4 h hypoxia (the Emax of NE was increased from 3.444 mN to 7.643 mN, P<0.01). ③At 10 min hypoxia, Ang-2 could decrease the tyrosine phosphorylation of Tie-2 from 0.040 3 to 0.012 3(P<0.01), and at 4 h hypoxia, Ang-1 could decrease the protein expression of Tie-2 from 0.227 6 to 0.085 1(P<0.01), and decrease the tyrosine phosphorylation of Tie-2 from 0.143 7 to 0.035 9(P<0.01). ④The NO concentration in the cells mixture was significantly increased in the early hypoxia, and the increase could be inhibited by Ang-2 and Tie-2 inhibitor(P<0.01); in the late hypoxia, the NO concentration was further increased, and could be inhibited by Ang-1 and Tie-2 inhibitor(P<0.01). CONCLUSION Ang-1 and Ang-2 regulate the biphasic change of vascular reactivity after hemorrhagic shock in rats through Tie-2 receptor.