Aim To clarify the relation of expression change of tumor necrosis factor-α (TNF-α) and angiotensin Ⅱ (AngⅡ)in hypertrophic mayocardial on stress load. Methods Sampling blood and extirpate heart after 42 days in the cardiac hypertrophy model of exceed stress load were made by abdomen aorta-constriction; determining hypertrophic exponent and the concentration of AngⅡin the plasma and myocardium by Ratio-immunity; determining TNF-α in serum and left ventricle by enzyme-linked immunoadsordent assay. Results Left ventricle showed obvious hypertrophy after operation 42 days; the concentration of TNF-α and AngⅡ in myocardium heighten 6 folds and 1 fold than controls (p<0.01); Being treated by Captopril can restrain the progress of left ventricle hypertrophy after operation and descend the content of TNF-α in myocardium 64.14% (p<0.01), but can not descend to the level of sham-operated group (p<0.01). Being the content of AngⅡ descend 45.73% (p<0.01)and had no marked significance to the level of sham-operated group. Conclusions The activation of cardiac renin-angiotensin system (RAS) by excess stress load result to heighten TNF-α in myocardium and it is probably one of the major adjusting path of myocardial hypertrophy.