Angiotensin‐(1‐7) [Ang‐(1‐7)] has been shown to play a significant role in the pathogenesis of lung inflammation via Mas receptor; however, its effect in chronic obstructive pulmonary disease (COPD) remains unknown. To explore the effect of Ang‐(1‐7) on a cigarette smoke (CS) exposure‐induced COPD model, 40 C57BL/6J mice were divided into four groups (n = 10) and exposed to air or CS for 8 weeks. After that, they were treated with saline or Ang‐(1‐7) at 0.3 mg/kg for 2 weeks by subcutaneous infusion using osmotic pump. The day following drug/vehicle challenge, lung function was examined and bronchoalveolar lavage (BAL) was performed. Chemokine (C–X–C motif) ligand 1, interleukin‐6, and tumor necrosis factor‐α protein levels in BAL fluid were determined using ELISA; the corresponding mRNA levels in lung tissues were measured using RT‐PCR. Mas1 receptor, pIκBα, IκBα, nuclear NF‐κB‐p65 protein, pERK1/2, ERK2, pp38, and p38 proteins expression in lung tissues were examined by immunohistochemical staining and western blotting. Ang‐(1‐7) challenge had no effect on the decreased lung function and emphysema induced by CS exposure. However, Ang‐(1‐7) treatment blocked CS exposure‐induced lung inflammatory responses and lung fibrosis, as determined by Masson's Trichrome staining. Exposure to CS for 8 weeks caused irreversible loss of lung function and emphysema, which could not be reversed by Ang‐(1‐7) treatment. Thus, the beneficial effect of Ang‐(1‐7) may be confined to pulmonary inflammation and fibrosis.