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肺血管局部的肾素血管紧张素系统在缺氧性肺动脉高压的发生中所起的作用尚不清楚。为此，动态观察了缺氧对培养的新生小牛肺动脉内皮细胞（ＰＡＥＣ）的血管紧张素转换酶（ＡＣＥ）活性的影响。结果发现：培养的ＰＡＥＣ在２．５％Ｏ２缺氧１．５ｈ末，培养液ＡＣＥ活性明显增高（与常氧组及０％Ｏ２组相比Ｐ＜０．００１）；随缺氧时间延长，３ｈ～１２ｈ，ＡＣＥ活性与１．５ｈ相比有所降低，但仍高于常氧组（Ｐ＜０．０５）；２４和４８ｈ，ＡＣＥ活性又大幅度升高（与常氧组及０％Ｏ２相比Ｐ＜０．００１）。０％Ｏ２缺氧条件下，ＡＣＥ活性仅在６ｈ和１２ｈ高于常氧组，而在２４ｈ低于常氧组（Ｐ＜０．０５），其它时点与常氧组相比差异不明显。０％Ｏ２条件下培养２４ｈ后，ＰＡＥＣ细胞内的ｃＧＭＰ含量明显降低（与常氧组相比Ｐ＜０．０５）。上述结果表明缺氧可引起ＰＡＥＣ的ＡＣＥ活性改变，这种改变可能参与缺氧性肺动脉高压的发生过程
The role of the renin-angiotensin system in the pulmonary vascular region in the pathogenesis of hypoxic pulmonary hypertension is unclear. To this end, the effect of hypoxia on angiotensin-converting enzyme (ACE) activity in cultured neonatal calf pulmonary artery endothelial cells (PAECs) was dynamically observed. The results showed that: PAEC cultured in 2.5% O2 hypoxia 1.5h end, the activity of ACE activity was significantly increased (compared with normoxia group and 0% O2 group P <0.001); with hypoxia time, Compared with normoxia group (P <0.05), ACE activity decreased significantly from 3h to 12h (P <0.05) O2 vs. P <0.001). Under 0% O2 hypoxia, ACE activity was higher than normoxia group only at 6h and 12h, but lower than normoxia group at 24h (P <0.05), but no significant difference at other time points compared with normoxia group. After cultured in 0% O2 for 24 h, the content of cGMP in PAEC cells was significantly decreased (P <0.05 compared with normoxia group). These results suggest that hypoxia can cause changes in PAEC ACE activity, this change may be involved in the process of hypoxic pulmonary hypertension