Hyperlipidemia can be harmful to the lung and beta(3)-adrenoceptor agonist can improve lipid metabolism disorders. In this study, we aim to investigate the effects or beta(3)-adrenoceptor activation On the interactions of adrenoceptors and angiotensin II receptors in aged apolipoprotein E gene knockout (ApoE(-/-)) mouse lung. Ten wild type C57BL/6J mice were included as normal control, 40 ApoE(-/-) mice were randomly divided into hyperlipidemia model (saline), low dose and high dose beta(3)-adrenoceptor agonist and beta(3)-adrenoceptor antagonist groups. After 26 weeks or high-fat diet, treatments were given for 12 weeks. Total cholesterol (TC), triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C) were examined by an automatic biochemical analyzer. Quantitative real-time PCR and Western blot were used to analyze the mRNA and protein expression of alpha(1A-), alpha(1B-) alpha(2A-), beta(1-), beta(2-), beta(3-) adrenoceptors and angiotensin II type 1 and type 2 receptors in lung. We found that beta(3)-adrenoceptor agonist could decrease TG, TC and LDL-C in aged ApoE mice (P<0.01) and down-regulate the expressions of alpha(1A-) alpha(2A)-Aadrenoceptors and angiotensin II type 1 receptor which were significantly increased in model mice (P< 0.01, P< 0.05). Compared with model mice, un-. beta(3)-adrenoceptors and angiotensin 11 type 2 receptor expressions were increased in beta(3)-adrenoceptor agonist-treat mice (P < 0.01, P < 0.05). These findings suggest that the expressions of adrenoceptors and angiotensin II receptors in lung are regulated towards adverse directions after taking beta(3)-adrenoceptor agonist, which shows there are interactions between beta(3)-adrenoceptor and other adrenoceptor subtypes and angiotensin II receptors. These interactions may play a protective role in lung under condition of hyperlipidemia. (C) 2014 Elsevier By. All rights reserved.