Abstract
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. 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. 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. 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.
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