Objective：To evaluate the in vivo and in vitro effects of Larginine (LArg) on cardiac hypertrophy and the related mechanisms. Methods: (1) In vivo study, rats were divided into shamoperation group, operation group, Larginine (LArg) group, and NnitroLarginine methyl ester (LNAME) group.Coarctation of abdominal aortic artery was performed in rats of the operation group,LArg group and LNAME group. The total protein level in the heart, the heart rate and blood pressure were all determined; cardiac nitric oxide (NO) content was detected by colorimetric method; cardiac ATⅡ content was determined by radioimmunoassay; and the expression of angiotensin converting enzyme (ACE) mRNA was determined by RTPCR. (2) In vitro study, primarily cultured cardiomyocytes were divided into control group, Angiotensin Ⅱ (ATⅡ)treated group, LArg treated group, and LNAME treated group. RTPCR was used to examine the mRNA expression of inducible NO synthase (iNOS), ATⅡ receptor type 1 (ATR1) and ATR2; Western blotting as employed to examine the iNOS protein expression. Results: (1) LArg increased the content of NO in animals of the operation group, decreased the content of ATⅡ, total protein synthesis, ratio of left ventricle mass/body mass, and expression of ACE mRNA; and LNAME could block the above effect of LArg. (2) Compared with ATⅡ group, ATⅡ+LArg higher content of NO, higher expression of iNOS mRNA and protein, and lower ATR1 mRNA level; the above indices were similar between ATⅡ+LArg+LNAME group and ATⅡ group. The expression of ATR2 mRNA was not significantly different between all the groups. (3) Multiple stepwise regression analysis revealed no relationship of regression between total protein level with blood pressure level or the heart rate. Cardiac NO and ATⅡ contents could serve as predictors for total protein level in the heart. (4) Cardiac NO content was negatively correlated with the cardiac ATⅡ content and ACE and ATR1 expression level.Conclusion: (1) The development of cardiac hypertrophy is closely related to cardiac NO and ATⅡ levels. (2) LArg can increase cardiac NO content through enhancing myocardial iNOS expression; NO can reduce ATⅡ production in myocardiocytes and can inhibit the formation of cardiac hypertrophy by reducing the expression of ACE and ATR1. (3) ATR2 does no participate in the above process.