Abstract: ObjectiveTo investigate the role of apoptosis played in myocardial hypertrophy and the effect of L-arginine (L-Arg) on the pathogenesis.Methods36 rats were randomly divided into the control group, model group and L-Arg treating group. The animal model of over-loading myocardial hypertrophy was made, and systolic blood pressure (SBP)and the cardiac indexes were measured, spectrophotography and flow cytometry were used to detect the content of nitric oxide (NO), activity of superoxide dismutase (SOD) and apoptosis rate.ResultsIn the model group, SBP, cardiac indexes and myocardial apoptosis rate increased, the content of NO and activity of SOD decreased compared with the control group. While, in the L-Arg treating group, SBP, cardiac indexes and apoptosis rate decreased, the content of NO and the activity of SOD increased compared with the model group.ConclusionMyocardial apoptosis may play an important role in the pathogenesis of myocardial hypertrophy and cause the losing of myocardial cells. L-Arg induces the increasing production of NO and inhibits myocardial apoptosis through increasing the activity of SOD.

Key words: myocardial hypertrophy, nitric oxide, L-arginine (L-Arg), apoptosis