Objective:To investigate in chronic hibernating myocardium in rabbits and the influence and significance of captopril, betaloc, valsartan in angiotensin Ⅱ subtype 1 receptor(AT1R), angiotensin Ⅱ subtype 2 receptor(AT2R), extracellular signal regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase(JNK). Methods: The model of chronic hibernating myocardium(CHM) was established. The changes of AT1R, AT2R, ERK1/2, JNK in different groups were assessed by western blotting and immunohistochemistry. Results: The amount of AT1R decreased while AT2R increased in the CON group compared with in sham group, and both AT1R and AT2R decreased in drug groups compared with the CON group. The content of ERK had no change in each group, while that of“expression” p-ERK increased in CON group compared with in sham group, and was lower in drug intervention groups than in CON and sham groups. The contents of JNK and p-JNK decreased in CON and drug intervention groups compared with in sham group. The protein levels of JNK, p-JNK in drug intervention groups were lower than in the CON group. Three drugs can inhibit interstitial fibrosis and reduce apoptotic cells. The expression levels in the groups(with different doses) had statistical difference as well as between groups of captopril and other drugs; however the results between betaloc and valsartan had no significant difference. Conclusion: AT1R, AT2R may be the upper stream receptor of ERK and JNK and may participate in generation and evolution of CHM. Captopril, valsartan and betaloc may preserve CHM by inhibiting AT1R, AT2R and JNK activity. Objective: To investigate in chronic hibernating myocardium in rabbits and the influence and significance of captopril, betaloc, valsartan in angiotensin Ⅱ subtype 1 receptor (AT1R), angiotensin Ⅱ subtype 2 receptor (AT2R), extracellular signal regulated kinase 1/2 (ERK1 / The changes of AT1R, AT2R, ERK1 / 2, JNK in different groups were assessed by western blotting and immunohistochemistry Results: The amount of AT1R decreased while the CON group compared with in sham group, and both AT1R and AT2R decreased in drug groups compared with the CON group. The content of ERK had no change in each group, while that of “expression ” p-ERK increased in CON group compared with in sham group, and was lower in drug intervention groups than in CON and sham groups. The contents of JNK and p-JNK decreased in CON and drug intervention groups compared with in sham group. The pro tein levels of JNK, p-JNK in drug intervention groups were lower than in the CON group. Three drugs can inhibit interstitial fibrosis and reduce apoptotic cells. The expression levels in the groups (with different doses) had statistical difference as well as between groups of captopril and other drugs; however the results between betaloc and valsartan had no significant difference. Conclusion: AT1R, AT2R may be the upper stream receptor of ERK and JNK and may participate in generation and evolution of CHM. Captopril, valsartan and betaloc may preserve CHM by inhibiting AT1R, AT2R and JNK activity.