Aim To observe the change of endothelin content and to explore the effects of vascular calcification on endothelin expression on the model of vascular calcification in rats induced by vitamin D 3 plus nicotine and calcified vascular smooth muscle cells induced by β glycerophosphate. Methods Arterial calcification of Sprague Dawley rats was induced by vitamin D 3 plus nicotine (VDN). Calcification of cultured rat vascular smooth muscle cells (VSMCs) was prepared by incubation with β glycerophosphate. Calcification was confirmed by Von Kossa staining, measurerment of calcium content, 45 Ca 2+ accumulation and alkaline phosphatase (ALP) activity of intracellular and vascular tissue. Endothelin levels in the plasma, vascular tissue and medium were measured by using radioimmunoassary. Endothelin mRNA level was determined by using competitive quantitative reverse transcription polymerase chain reaction. Results The results showed that the content of calcium, 45 Ca 2+ uptake and alkaline phosphatases activity in calcified VSMCs were increased by 118%, 174% and 7 fold respectively (all p<0.01), compared with control VSMCs. Content of endothelin in medium was increased by 35% (p<0.01). It was found that the amount of endothelin mRNA was elevated by 120% (p<0.01) compared with control. The calcium content, 45 Ca 2+ accumulation and ALP activity in calcified arteries were increased by 5.0 fold, 1.4 fold and 1.4 fold respectively (p<0.01), compared with control. Furthermore, it was showed that endothelin 1 levels in plasma and arteries tissues increased 102% and 103% respectively, compared with control (p<0.01). The amount of endothelin mRNA in calcified aorta was elevated by 22% (p<0.01) compared with control. However, the content of calcium, 45 Ca 2+ uptake and ALP activity in VDN plus endothelin receptor inhibitor groups were decreased by 33%, 36.7% and 40.4% respectively (p<0.01), compared with VDN group alone. Conclusions These results showed that in calcified artery and VSMCs the production of endothelin was increased,and the gene expression of endothelin was up regulated. The Bosentan (inhibitor of endothelin receptor) significantly reduced the vascular calcification. These results suggested that endothelin could play a role in the pathogenesis of vascular calcification.