Aim and Methods Endothelin 1 (Et-1) is a potent vasoconstriction peptide which was firstly isolated from the conditioned medium of porcine aortic endothelial cells. Hypoxia can induce Et-1 gene expression in rat lung tissue and pulmonary artery. In order to assess the role of Et-1 in processes of pulmonary vasoconstriction and pulmonary vessel remodeling induced by hypoxia, the effects of ET-1 on contraction of pulmonary artery in rat and proliferation of pulmonary arterial smooth muscle cells in cultured of rabbit are investigated. Results ET-1 at concentrations ranged from 1× -9 to 12×10 9 mol/L caused-depended contration of vessel rings of rat pulmonary artery (r=0.935,P<0.05). When rabbit pulmonary arterial smooth muscle cells were cultured in the presence of 0.5% fetal calf serum (FCS), ET-1 at concentrations ranged from 1×10 11 to 1×10 -8 mol/L also stimulated 3 H-thymidine and 3 H- leucine incorporation in confluent quiescent monolayers in a dose-dependent manner (r=0.756 and 0.840, respectively), with EC50 being 10.87 nmol/L and 8.54 nmol/L. Conclusion Endothelin-1 may play a certain role in the hypoxic pulmonary hypertension.