β‐blockers, especially selective β1‐blockers, are often used to treat cardiovascular disease, even when complicated by chronic obstructive pulmonary disease. The association of β‐blocker selectivity and treatment effects is disputed, and the curative as well as side effects of various antagonists may differ. We investigated the effect of 1‐month treatment with the selective β1‐blocker metoprolol and nonselective β‐blocker propranolol on pulmonary function and pathology in a 4‐month rat model of passive cigarette‐smoke exposure and explored a potential mechanism. Lung function and general pathological changes were evaluated after 4‐month cigarette‐smoke exposure, with metoprolol and propranolol treatment during the last month. The levels of cytokines and mucin in bronchoalveolar lavage fluid were detected by ELISA. β1 and β2‐adrenergic receptor expression in the lung was detected by immunohistochemistry and western blot analysis. Chronic treatment with metoprolol and propranolol did not exacerbate peak expiratory flow or intra‐airway pressure in rats exposed to cigarette smoke. Propranolol significantly attenuated inflammatory cell infiltration, cytokine levels (tumor necrosis factor α and interleukin 8) in bronchoalveolar lavage fluid or mucus secretion; metoprolol reduced only smooth muscle proliferation. Moreover, propranolol treatment was associated but not significantly with restoring β2‐adrenergic receptor expression in the airway epithelia. Propranolol had a more beneficial effect on cigarette smoking‐induced lung damage than metoprolol in a smoking rat model and may be involved in restoring endogenous β2‐adrenergic receptor density in the airway epithelial cells. This article is protected by copyright. All rights reserved.