Objective：To investigate the effects of AngII antagonist valsartan on airway inflammation and airway hyperresponsiveness（AHR） in asthmatic rats. Methods: Fifty Wistar rats were divided into 5 groups, group A（normal control group）, group B（asthma group）, group C ［treated with valsartan, 15mg／（kg·d）］, group D［treated with valsartan, 30 mg／（kg·d）］，and group E ［treated with valsartan, 50 mg／（kg·d）］, with 10 rats in each group. Pulmonary function tests were performed to evaluate the airway responsiveness, and bronchial alveolar lavage fluid（BALF） was used to analyze the total cell and eosinophil（EOS） counts. Results: Compared with group A , group B had an increased count of total cell and EOS in BALF（P ＜ 0.05，P ＜ 0.01) . Compared with group B, group C, D, E showed a decreased count of total cell and EOS in BALF（P ＜ 0.05-0.01). Compared with group C, group D had a significantly decreased count of total cell and EOS（P ＜ 0.01) in BALF. After stimulation of methicholine with accelerated concentrations（40，80，160 μg／ml）, the mean expiratory resistance（Re） of group B was higher than that of group A, C, D, E（P < 0.05). When the concentration of methicholine was 320 μg／ml, the asthmatic group showed a significant difference. Conclusion: Valsartan may inhibit airway inflammation and reduce airway responsiveness by suppressing AT1 receptors.