[Effect of angiotensin II on the expression of aquaporin 1 in lung of rats following acute lung injury].
OBJECTIVE
To investigate the effect of angiotensin II (Ang II) on the expression of aquaporin 1 (AQP1) in lung of rats with acute lung injury (ALI) and the role of Ang II in the formation of lung edema.


METHODS
Forty healthy Sprague-Dawley (SD) rats were randomly divided into sham-operated group, model group, Ang II receptor blocker pretreatment group, and Ang II receptor blocker treatment group according to random digits table, with 10 rats in each group. ALI model of rats was reproduced with administration of endotoxin after hemorrhagic shock. In rats of pretreatment group Ang II receptor blocker 30 microg/kg was given 30 minutes before lipopolysaccharide (LPS) injection; rats in treatment group Ang II receptor blocker 30 microg/kg was given 30 minutes after LPS injection; rats in model group received 30 microg/kg normal saline 30 minutes before and after LPS injection. Rats were sacrificed 6 hours after model establishment, samples of venous blood and lung tissue were collected, radioimmunoassay was used to measure the level of tumor necrosis factor-alpha (TNF-alpha) in serum and the expression of Ang II in lung tissue, ratio of wet to dry (W/D) weight of lung tissue was calculated, reverse transcription-polymerase chain reaction was used to measure the expression of AQP1 mRNA in lung tissue.


RESULTS
Compared with rats of sham-operated group, the level of TNF-alpha in venous blood, W/D ratio and the expression of Ang II in lung tissue increased significantly, the expression of AQP1 mRNA in lung tissue decreased significantly in rats of ALI. Compared with rats of model group, the level of TNF-alpha in venous blood (microg/L) decreased significantly (4.79+/-0.24, 5.55+/-0.36 vs. 6.34+/-0.31, both P<0.05), W/D ratio decreased significantly (4.34+/-0.23, 4.85+/-0.20 vs. 5.41+/-0.26, both P<0.05), the expression of AQP1 mRNA in lung tissue increased significantly (0.854+/-0.067, 0.727+/-0.081 vs. 0.358+/-0.071, both P<0.05), and the expression of Ang II in lung tissue (ng/g) decreased to some extent (172.19+/-15.82, 202.82+/-20.47 vs. 245.88+/-26.31), but without statistical significance (both P>0.05) in rats of pretreatment group and treatment group. The expression of AQP1 mRNA was negatively correlated with both the level of Ang II and W/D ratio (r1=-0.782, r2=-0.726, both P<0.05).


CONCLUSIONS
During ALI, Ang II may downregulate the expression of AQP1 mRNA in lung tissue directly or through inflammatory mediators, Ang II may play a role in the formation of lung edema.
Cao
Chun-shui
CS
Department of Emergency Medicine, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China.
Yin
Qin
Q
Huang
Liang
L
Zhan
Zuan
Z
Yang
Ji-bin
JB
Xiong
Hua-wei
HW
D055371:Acute Lung Injury / Q000378:metabolism* / Q000473:pathology; D000804:Angiotensin II / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D051398:Aquaporin 1 / Q000378:metabolism*; D004195:Disease Models, Animal; D008168:Lung / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley
C496022:Aqp1 protein, rat; D000804:Angiotensin II; D051398:Aquaporin 1