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Objective:To investigate the effects of sodium ferulate(SF) on myocardial hypertrophy of rat and explore the protective mechanism.Methods:The myocardial hypertrophy was induced by 0.1μmol·L-1 Ang II. The cytoactive was detected by MTT. The cultured cardiomyocytes from Sprague Dawley neonate rats were randomly divided into normal,model,L-arginine(L-arg 1000μmol·L-1) group and SF(50,100,200μmol·L-1) group.To observe whether SF had nonspecifi c injurious effect on the cells,SF 200μmol·L-1was added into the normal cardiomyocytes and to determine whether the effect of SF on cardiomyocyte hypertrophy was associated with NO release,another two groups were established. NG-nitro-L-arginine-methyl ester(L-NAME) 1500μmol·L-1 combined with SF 200μmol· L-1 or L-arg 1000μmol·L-1,respectively. Cardiomyocyte hypertrophy was confirmed by observing the histological changes and the measurements of cell diameter,protein content and ANF andβ-MHC mRNA expression of the cells.The levels of NO,NOS and eNOS activity,the contents of cGMP and cAMP. The expression of eNOS were detected by Real time PCR and Western blotting.Results:① SF (50,100,200μmol·L-1) had no obvious side effect on cultured neonatal rat cardiomyocytesin vitro. In the group added 0.1μmol·L-1AngⅡ alone,the cells displayed swollen,with undistinguishable border;the diameter and protein content of cardiomyocytes was increased remarkably,and the expression of ANF andβ-MHC mRNA were up-regulated by AngⅡ. SF and L-arg could ameliorate the cardiomyocyte hypertrophy which can be inhibit by L-NAME.② Compared with normal group, 0.1μmol· L-1Ang II could decrease the NO content,NOS and eNOS activity in supernatant of cultured cardiomyocytes,decrease the content of cGMP and increase the content of cAMP incardiomyocytes,up-regulation the expression of eNOS.SF-H and L-arg administrated could siginifi cantly ameliorate these changes.Conclusion:SF can inhibit cardiomyocyte hypertrophy induced AngⅡ in rats. The probable mechanism involved to promote NO-cGMP signaling pathway and up-regulate the expression of eNOS .