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缺氧是否通过影响血管内皮细胞的分泌功能而参与缺氧性肺动脉高压的发生尚不清楚。本实验动态观察了缺氧对培养的新生小牛内皮细胞（ＰＡＥＣ）的血管紧张素Ⅱ（ＡＴⅡ）分泌的影响。结果发现：２．５％Ｏ２缺氧早期（１．５ｈ），ＰＡＥＣ的ＡＴⅡ分泌增加（Ｐ＜０．０１ｖｓ常氧组），缺氧后期与常氧组无明显差别；０％Ｏ２缺氧早期（１．５－６ｈ），ＡＴⅡ分泌明显降低（Ｐ＜０．０１ｖｓ常氧组及２．５％Ｏ２组），后期ＡＴⅡ分泌明显增高（Ｐ＜０．０１ｖｓ常氧组及２．５％Ｏ２组）；无论缺氧还是常氧条件下，ＮＯ供体ＳＩＮ１显著抑制ＡＴⅡ的分泌（Ｐ＜０．０１），而内源性ＮＯ抑制剂硝基精氨酸则明显促进ＡＴⅡ分泌（Ｐ＜０．０１）；０％Ｏ２缺氧２４ｈ后，ＰＡＥＣ细胞内ｃＧＭＰ含量明显降低（Ｐ＜０．０５）。上述结果表明缺氧可通过抑制ＰＡＥＣ的内源性ＮＯ产生而促进ＡＴⅡ的分泌，ＰＡＥＣ自分泌的改变可能参与缺氧性肺动脉高压的发生过程。
Whether hypoxia is involved in the pathogenesis of hypoxic pulmonary hypertension by influencing the secretion function of vascular endothelial cells is still unclear. This experiment dynamically observed the effect of hypoxia on the secretion of angiotensin Ⅱ (ATⅡ) in cultured neonatal calf endothelial cells (PAEC). The results showed that ATⅡ secretion of PAEC increased in 2.5% O2 hypoxia (1.5h) (P <0.01vs normoxia group), there was no significant difference between hypoxia and normoxia group (1.5-6h), ATⅡ secretion was significantly decreased (P <0.01vs normoxia group and 2.5% O2 group), late AT Ⅱ secretion was significantly increased (P <0.01vs normoxic group and 2.5% O2 Group). Nitric oxide (NO) donor SIN1 significantly inhibited ATⅡ secretion (P <0.01) under both anoxic and normoxic conditions, whereas nitric arginine, an endogenous nitric oxide inhibitor, significantly promoted ATⅡ secretion (P <0.01). After 24h of 0% O2 hypoxia, the content of cGMP in PAEC cells was significantly decreased (P <0.05). These results suggest that hypoxia can promote the secretion of ATⅡby inhibiting the production of endogenous NO in PAEC. The change of PAEC autocrine may be involved in the pathogenesis of hypoxic pulmonary hypertension.