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Canadian Respiratory Journal
Volume 19 (2012), Issue 5, Pages 311-318
http://dx.doi.org/10.1155/2012/951025
Original Article

The Effect of Endogenous Angiotensin II on Alveolar Fluid Clearance in Rats with Acute Lung Injury

Jia Deng,1 Dao-xin Wang,2 Wang Deng,2 Chang-yi Li,2 and Jin Tong2

1Department of Respiratory Medicine, Second Affiliated of Chongqing Medical University, Chongqing, China
2Department of Medicine, Second Affiliated of Chongqing Medical University, Chongqing, China

Copyright © 2012 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

BACKGROUND: In acute lung injury (ALI), angiotensin II (Ang II) plays a vital role in the stimulation of pulmonary permeability edema formation through the angiotensin type 1 (AT1) receptor. The effect of Ang II on alveolar fluid clearance (AFC) in ALI remains unknown.

METHODS: Sprague Dawley rats were anesthetized and intratracheally injected with 1 mg/kg lipopolysaccharide (LPS), while control rats received saline. The AT1 receptor antagonist ZD7155 was injected intraperitoneally (10 mg/kg) 30 min before LPS administration. The lungs were isolated for AFC measurement, and alpha-epithelial sodium channel (ENaC) messenger RNA and protein expression were detected by reverse-transcription polymerase chain reaction and Western blot.

RESULTS: LPS-induced ALI caused an increase in Ang II levels in plasma and lung tissue but a decrease in AFC. The time course of Ang II levels paralleled that of AFC. Pretreatment with ZD7155 prevented ALI-induced reduction of AFC. ZD7155 also reversed the ALI-induced reduction of beta-ENaC and gamma-ENaC levels, and further decreased alpha-ENaC levels.

CONCLUSIONS: These findings suggest that endogenous Ang II inhibits AFC and dysregulates ENaC expression via AT1 receptors, which contribute to alveolar filling and pulmonary edema in LPS-induced ALI.