Aim To investigate the effects of asymmetric dimethylarginine on the expression of soluble intercellular adhesion molecule-1 (sICAM-1), nitric oxide (NO) and endothelin-1 (ET-1) in human umbilical vein endothelial cells (hUVEC), and observe whether L-arginine (L-arg) of different dosage can antagonize the effects of ADMA. Methods ADMA or ADMA plus L-arg was incubated with hUVEC for 24 h. The levels of sICAM-1, ET-1 and NO in conditioned medium were measured by means of Enzyme-Linked Immunosorbent, Griess and Assay radio-immunosorbent. Results ADMA can increase hUVEC to express sICAM-1, ET-1 and decrease hUVEC to generate No in a concentration-dependent manner (p<0.05, respectively), but these effects were gradually dismissed after giving the increasing dosage of L-arg. Compared with the control group, the group of ADMA 1 μmol/L had no significant difference in the expression of sICAM-1, NO and ET-1. Except this group, the other four ADMA groups all had significant difference compared with the control group (p<0.05, respectively). Among the five ADMA groups, they all had significant difference each other (p<0.05, respectively). When the added L-arg/ADMA ratio is big enough (L-arg/ADMA>100), there are no more improvements of endothelial function. The levels of sICAM-1, NO and ET-1 in conditioned medium were significantly correlated with the levels of ADMA (r=0.943, -0.937, 0.934, p<0.01, respectively). Conclusion ADMA can induce endothelial dysfunction by means of increasing endothelial cells to express sICAM-1, ET-1 and decreasing endothelial cells to generate NO. The degree of endothelial dysfunction is significantly correlated with the levels of ADMA. Giving exogenous L-arginine can antagonize the effects of ADMA. Effective measures to regulate the plasma level of ADMA may be the new aim to improve endothelial function and treat cardiovascular disease.