AimTo explore the roles of regulating energy metabolism and mechanism of adenosine A1 receptor agonist inhibiting myocardial hypertrophy by means of 2-chlorinated adenosine (2-CADO) on isoproterenol induced myocardial hypertrophy in rats.MethodsHigh-dose isoproterenol subcutaneous injection to rats were used to establish myocardial hypertrophy model.Forty Sprague-Dawley rats were randomly divided into four groups with ten rats for each group: control group, isoproterenol induced myocardial hypertrophy group, isoproterenol induced myocardial hypertrophy＋2-CADO (6 mg/(kg·d), intraperitoneal injection) group, isoproterenol induced myocardial hypertrophy＋propranolol (28 mg/(kg·d), per os) group.Rats began to medicate at the second day after myocardial hypertrophy model establishment for 8 weeks.The whole heart quality index (HMI)and left heart quality index (LVMI) were detected.Left ventricular tissue was taken to observe the changes of TDM by Masson staining.Hydroxyproline (Hyp) content was determined by alkaline hydrolysis.Myocardial tissue lactate (LA) and free fatty acid (FFA) content were detected by UV spectrophotometry.Mitochondrial membrane potential (MMP) was detected by laser scanning confocal microscope.ResultsCompared with control group, in myocardial hypertrophy group HMI and LVMI were higher, the contents of Hyp, LA and FFA from left myocardial tissue were significantly increased and MMP decreased by 44%.Compared with myocardial hy-pertro phy group, in myocardial hypertrophy＋2-CADO group and myocardial hypertrophy＋propranolol group HMI, LVMI and the contents of Hyp, LA and FFA reduced, MMP increased by 50%.ConclusionsAdenosine receptor agonist 2-CADO can inhibit myocardial hypertrophy induced by isoproterenol, the mechanism may be related to improving cardiac energy metabolism and preserving MMP.