Objective To investigate the effect of long-acting nitrate on the left ventricular function and the expression of α1- and β-adrenergic receptors subtypes in the lung tissue of rats with myocardial infarction-induced chronic heart failure (CHF). Methods Ninety inbred male Wistar rats were divided into normal control group (N group, n＝9), sham-operation group (SH group, n＝8) and heart failure (HF) model group (n＝73). The HF model was successfully induced by ligating left anterior descending (LAD) artery in 44 rats. In 4 weeks after operation, the rats from the model group were divided into 5 groups, HF group (HF group, n＝9), low-dose nitrate group (LN group, n＝9), high-dose nitrate group (HN group, n＝9), positive medicine (olmesartan) control group (OL group, n＝9) and high dose nitrate combined with positive medicine group (HN＋OL group, n＝8). The medication was given by gastric gavage for 6 weeks. Cardiac function was examined by echocardiography before and after the treatment, and the expression of β1-AR, β2-AR, β3-AR, α1A-AR, α1B-AR, and α1D-AR at mRNA and protein levels in the lung parenchyma was determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. Results After the treatment, left ventricular ejection fraction (LVEF) was markedly higher in HN, OL and HN＋OL groups than in HF group (P＜0.05). Compared with SH group, the expression of α1A-AR, α1B-AR, and β2-AR was significantly up-regulated (P＜0.05), and that of β1-AR and β3-AR was down-regulated in HF group (P＜0.05). Compared with HF group, the expression of α1A-AR, α1B-AR, and β2-AR was significantly down-regulated, and the expression of β1-AR and β3-AR was significantly up-regulated in HN, OL, and HN＋OL groups (P＜0.05). Furthermore, there was significant difference in the expression of above subtypes between the OL group and HN＋OL group (P＜0.05). No obvious difference was seen in the expression level of α1D-AR among all groups. Conclusion Long-acting nitrate therapy remarkably improves LVEF in CHF rats induced by myocardial infarction, reverses the lung expression levels of α1- and β-AR subtypes to normal, and exerts a beneficial effect on the protection of lung function.