Objective To research the effect of exogenous angiotensin Ⅱ (Ang Ⅱ ) on alveolar fluid clearance (AFC) and alveolar epithelial sodium channel (ENaC) expression in rats. Methods Fifteen healthy Sprague-Dawley (SD) rats were randomly divided into control group, Ang Ⅱ group and Ang Ⅱ type 1(AT1) receptor blocker ZD7155 pretreatment group, with 5 rats in each group. Exogenous Ang Ⅱ10 μg · kg 1 · min-1 was administered by micro pump via catheter in left jugular vein in Ang Ⅱ group and ZD7155 pretreatment group, whereas control group rats received only normal saline. ZD 7155 10 mg/kg was injected intraperitonealy 30 minutes before administration of exogenous Ang Ⅱ in ZD7155 pretreatment group. The pathological changes in lung were observed after 6 hours. AFC was estimated by Evans-blue labeled 5％ albumin. The mRNA and protein expression of ENaC were determined by semi-quantitive reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. Results AFC in Ang Ⅱgroup was significantly lower than that of control group [(6.16± 3. 01)％ vs. (16. 10± 3. 46)％, P＜0. 01],and AFC in ZD7155 pretreatment group was significantly higher than that of Ang Ⅱ group [(10. 60±2.05)％vs. (6. 16 ± 3. 01)％, P＜0. 05]. α-ENaC mRNA expression was significantly increased in Ang Ⅱ group compared with control group (0. 663 ± 0. 068 vs. 0. 236± 0. 030, P＜ 0. 01), but significantly decreased in ZD7155 pretreatment group when compared with Ang Ⅱ group (0. 386 ± 0. 061 vs. 0. 663 ± 0. 068, P＜0. 01). There was no significant difference in β-ENaC and γ-ENaC mRNA expression among three groups.Compared with control group, α-ENaC protein was significantly increased in Ang Ⅱ group (0. 343±0. 053 vs.0. 145±0. 030, P＜0. 01), but β-ENaC and γ-ENaC proteins were significantly decreased (β-ENaC: 0. 286±0.038 vs. 0.512±0.055, γ-ENaC: 0.144±0.040 vs. 0.460±0.066, both P＜0.01). Compared with Ang Ⅱ group, α-ENaC protein was significantly lower(0. 228± 0. 045 vs. 0. 343± 0. 053, P＜0. 01), whereas β-ENaC and γ-ENaC proteins were significantly higher (β-ENaC: 0. 358±0. 043 vs. 0. 286±0. 038, γ-ENaC:0. 220±0. 033 vs. 0. 144±0. 040, both P＜0. 05) in ZD7155 pretreatment group. Conclusion Exogenous Ang Ⅱ modulates ENaC expression of gene and protein by AT1 receptor pathway, attenuates AFC, and aggravates lung edema.%目的 探讨外源性血管紧张索Ⅱ (Ang Ⅱ)对大鼠肺泡液体清除及肺泡上皮钠通道(ENaC)表达的影响。方法 按随机数字表法将15只SD大鼠分为对照组、Ang Ⅱ组及Ang Ⅱ 1型受体阻滞剂ZD7155干预组，每组5只。Ang Ⅱ组和ZD7155干预组大鼠经左侧颈静脉置管后，微量泵持续泵入外源性Ang Ⅱ10 μg．kg-1．min-1；对照组泵入等量生理盐水。ZD7155干预组于泵入Ang Ⅱ前30 min经腹腔注射10 mg/kg ZD7155。6h后观察肺组织病理学改变；用伊文思蓝标记5％白蛋白法测定离体肺组织肺泡液体清除率(AFC)；用逆转录-聚合酶链反应(RT-PCR)测定ENaC mRNA表达，用蛋白质免疫印迹法(Western blotting)测定ENaC蛋白表达。结果 Ang Ⅱ组AFC较对照组显著降低[（6.16±3.01）％比(16.10±3.46)％，P＜0.01]，ZD7155干预组AFC较Ang Ⅱ组显著升高[（10.60±2.05）％比(6.16±3.01)％，P＜0.05]。Ang Ⅱ组α-ENaC mRNA表达较对照组显著升高（0.663±0.068比0.236±0.030，P＜0.01），ZD7155干预组α-ENaC mRNA表达较Ang Ⅱ组显著降低（0.386±0.061比0.663±0.068，P＜0.01）；β-ENaC及γ-ENaC的mRNA表达无明显差异。与对照组比较，Ang Ⅱ组α-ENaC蛋白表达显著增加(0.343±0.053比0.145±0.030，P＜0.01)，β-ENaC和γ-ENaC的蛋白表达显著降低（0.286±0.038比0.512±0.055，0.144±0.040比0.460±0.066，均P＜0.01）；与Ang Ⅱ组比较，ZD7155干预组α-ENaC蛋白表达显著降低(0.228±0.045比0.343±0.053，P＜0.01)，β-ENaC和γ-ENaC的蛋白表达显著升高(0.358±0.043比0.286±0.038，0.220±0.033比0.144±0.040，均P＜0.05)。结论 外源性Ang Ⅱ通过其1型受体途径调节ENaC基因及蛋白表达，减弱大鼠肺泡液体清除，加重肺水肿。
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