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内皮素（ＥＴ）是至今所发现的最强的内源性血管收缩肽，近年来发现ＥＴ－１能促进血管平滑肌细胞增殖。本研究表明ＥＴ－１对缺氧培养的肺动脉平滑肌细胞（ＰＡＳＭＣ）有剂量依赖的增殖作用，缺氧可促进ＰＡＳＭＣ的ＤＮＡ合成且增加ＥＴ－１的丝裂原作用。ＥＴ－１的丝裂原作用主要由其Ａ型受体（ＥＴＲ＿Ａ）所介导，ＥＴＲ＿Ａ的特异拮抗剂ＢＱ１２３可显著抑制缺氧以及缺氧与ＥＴ－１协同所产生的增殖作用，而且发现ＥＴＲ＿Ａ在缺氧培养的ＰＡＳＭＣ中的表达显著高于常氧对照组ＰＡＳＭＣ。本研究表明ＥＴ－１参与了缺氧性肺动脉结构重组，而缺氧可增强ＰＡＳＭＣ对ＥＴ－１的增殖反应性。
Endothelin (ET) is the strongest endogenous vasoconstrictor peptide discovered so far. ET-1 has been found to promote vascular smooth muscle cell proliferation in recent years. This study shows that ET-1 can dose-dependently proliferate hypoxic cultured pulmonary artery smooth muscle cells (PASMC). Hypoxia can promote DNA synthesis of PASMC and increase the mitogenic effect of ET-1. The mitogen effect of ET-1 was mainly mediated by its type A receptor (ETR_A). BQ123, a specific antagonist of ETR_A, significantly inhibited hypoxia and the synergistic effect of hypoxia and ET-1. ETR_A The expression of PASMC in hypoxic culture was significantly higher than that of normoxic control PASMC. This study shows that ET-1 is involved in the structural reorganization of hypoxic pulmonary artery, and hypoxia can enhance the proliferation of PASMC on ET-1 response.