Abstract: Abstract：Aim To investigate omapatrilat on endothelin-1 (ET-1)-induced cardiomyocyte hypertrophy in neonatal rats. Methods Isolated and cultured cardiomyocyte of neonatal Sprague-Danley (SD) rats were randomly divided into 6 groups: control, ET-1, OMA, ET-1＋OMA,ET-1＋OMA＋L-NAME and ET-1＋OMA＋HS-142-1. Nitric Oxide synthetase (NOS) activity was measured by Spectrophotometry. Intracellular cyclic GMP (cGMP) were measured by radioimmunoassay. [3H]-leu incorporation and PKC activity were evaluated by scintillation. Results Compared with the control group, 10-6mol/L ET-1 significantly increased the surface area, the activity of PKC and [3H]-leu incorporation of cardiomyocyte, decreased the activity of NOS and cGMP content (P < 0.01 for all); 10-7 mol/L OMA inhibited the above effects of ET-1 on cardiomyocyte (P < 0.01 v.s ET-1). L-NAME, HS-142-1 partially blocked the inhibitory effects of OMA ( P < 0.05). Conclusion The NO/cGMP and PKC may partially mediate the antiproliferation action of OMA in ET-1-induced cardiomyocyte hypertrophy.