Aim To explore effects and mechanism of panax notoginseng saponin (PNS) on hypertrophic myocardium caused by abdominal aorta constriction(AAC) in rats. Methods Rat left ventricular hypertrophy was induced by abdominal aorta constriction in 75 rats, and 15 rats were randomly taken as sham group. One week after surgery, rats were divided into 4 groups: model group (abdominal aorta constriction rats), low-dose PNS group (50 mg/kg), middle-dose PNS group (100 mg/kg) and high-dose PNS group (150 mg/kg). After accepting therapy for 11 weeks, the hemodynamics of all animals was detected the left ventricle was recorded to calculate left ventricular hypertrophic parameters including left ventricular hypertrophy index (HMI, the ratio of the heart and body weight and LVMI, the ratio of the left ventricular weight and body weight) pathological section was stained by hematoxylin-eosin(HE) the lactic acid (LAC) and free fatty acids(FFA) were measured the mRNA expression of heart atrial natriuretic peptide (ANP) was observed through reverse transcription-polymerase chain reaction (RT-RCR) the contents of adenosine triphosphate (ATP), adenosine diphosphate(ADP) and adenosine monophosphate (AMP) in rat were detected by high performance liquid chromatography (HPLC). Results Compared with the AAC model group, PNS was able to inhibit cardiac hypertrophy, ameliorate hemodynamics, the expression of atrial natriuretic peptide was decreased, the lactic acid (LAC) and free fatty acid (FFA) levels was decreased, and the content of ATP, ADP and AMP was largely increased. Conclusions PNS protection against left ventricular hypertrophy elicited by abdominal aorta constriction in rats is mediated, at least in part, via ameliorate energy metabolism.