[Effect of angiotensin II on expression of alveolar epithelial sodium channel in rat]

To research the effect of exogenous angiotensin II (AngII) on alveolar fluid clearance (AFC) and alveolar epithelial sodium channel (ENaC) expression in rats.

Fifteen healthy Sprague-Dawley (SD) rats were randomly divided into control group, AngII group and AngII type 1 (AT1) receptor blocker ZD7155 pretreatment group, with 5 rats in each group. Exogenous AngII 10 μg× kg(-1)×min(-1)was administered by micro pump via catheter in left jugular vein in AngII group and ZD7155 pretreatment group, whereas control group rats received only normal saline. ZD 7155 10 mg/kg was injected intraperitoneal 30 minutes before administration of exogenous AngII 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-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting.

AFC in AngII group 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 AngII group [(10.60 ± 2.05)% vs. (6.16 ± 3.01)%, P<0.05]. α-ENaC mRNA expression was significantly increased in AngII 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 AngII 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 AngII 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 AngII 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.

Exogenous AngII modulates ENaC expression of gene and protein by AT1 receptor pathway, attenuates AFC, and aggravates lung edema.