To investigate the effect of myocardial hypertrophy induced by pressure overload on autophagy of myocardial cells, a rat model of pressure overload is established by abdominal aortic stenosis. Body weight, heart weight and left ventricular weight are measured at different time points after operation and compared with control group. After hematoxylin-eosin (H.E) staining, electron microscopy is used to compare the area of myocardial cells between operation group and control group. After immunofluorescence labeling, laser confocal microscopy is used to observe and localize autophagy-related proteins. Western bolt is used to detect the expression of autophagy-related proteins. The results show that the tissue weight at 3 days after operation is significantly higher than that of the control group (P < 0.05). The results of H.E staining show that the area of myocardial cells is significantly higher than that of control group (P < 0.05). Immunofluorescence labeling show that LC3 increases significantly 3 days after operation. Moreover, Western blot show that the expression of LC3II/LC3I protein in rat cardiomyocytes is significantly higher than that in control group 3 days after operation (P < 0.05). The expression of p62 protein is significantly lower than that of control group (P < 0.05). The total protein levels of APMK and ACC in the operation group are not different from those in the control group, but the phosphorylation of AMPK (p-AMPK) and ACC (p-ACC) are significantly lower than those in the control group (P < 0.05) 3 days after operation. This suggests that pressure overload can lead to myocardial hypertrophy in rats. By affecting the expression of LC3 and p62 proteins and the phosphorylation of AMPK and ACC, autophagy of cardiomyocytes is enhanced.