Abstract: Objective To study the effect of TNF-α on renal vasoconstriction sensitivity. Methods A rat in vitro perfusion kidney model was established. Twenty eight male SD rats were randomly divided into A₁ group, A₂ group, B₁ group and B₂ group (7 in each group). Rats in the 4 groups underwent perfusion with Ca²⁺-free Kreb's solution, TNF-α and Ca²⁺-free Kreb's solution (100 μg/L), Ca²⁺-free Kreb's solution and 2-APB (30 µmol/L), TNF-α (100 μg/L) and Ca²⁺ -free Kreb's solution and 2-APB (30 µmol/L)respectively, and stimulated with 1nmol/L endothelin (ET). Then, kidney edema rate was calculated. Morphology and structure of glomeruli and renal tubules were observed. Results No significant difference was found in the basic perfusion pressure among the 4 groups (P＞ 0.05). Although the renal perfusion pressure was significantly higher than the basic perfusion pressure in A₁ and A₂ groups (P＜ 0.05), it was significantly higher in A₂ group than in A₁ group after ET stimulation (P＜ 0.05). Although the renal perfusion pressure was slightly higher in B₁ and B₂ groups, no significantly difference was found in the perfusion pressure and basic perfusion pressure between the two groups (P＞ 0.05). The kidney edema rate was lower than 30% in the 4 groups. No significant organic injury was observed in renal tissue sections after perfusion. Conclusion TNF-α can stimulate ET–induced renal vasoconstriction by up-regulating the IP3R.