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目的:观察卡托普利(Cap)抑制缺氧诱导的肺动脉平滑肌细胞(VSMC)增殖和胶原合成的作用,方法:采用细胞计数,[~3H]脱氧胸苷,[~3H]脯氨酸掺入和细胞内游离钙测定的方法。结果:卡托普利(Cap,1μmol·L~(-1))抑制缺氧诱导的VSMC中细胞数目,[~3H]脱氧胸苷和[~3H]脯氨酸掺入及细胞内游离钙的增高,较缺氧组分别降低了25％,36％,21％和16％,硝苯吡啶也具有上述抑制作用,Bay-K-8644促进VSMC中细胞数目,[~3H]脱氧胸苷和[~3H]脯氨酸掺入及细胞内游离钙的增高,分别增加35％,55％,36％,34％,这种作用可被Cap阻断。结论:Cap抑制缺氧诱导的肺动脉平滑肌细胞增殖和胶原合成,这可能与阻断L型钙通道有关。
AIM: To observe the effect of captopril on hypoxia - induced proliferation and collagen synthesis of pulmonary artery smooth muscle cells (VSMCs). Methods: Cell counting, [~ 3H] deoxythymidine, [~ 3H] Into and intracellular free calcium determination method. RESULTS: Cap (1 μmol·L -1) inhibited the cell number induced by hypoxia, the incorporation of [~ 3H] deoxythymidine and [~ 3H] proline and the intracellular free calcium , Which was reduced by 25%, 36%, 21% and 16% respectively compared with that in hypoxia group. Nifedipine also had the above inhibition. Bay-K-8644 promoted the number of VSMC cells, [~ 3H] proline incorporation and intracellular free calcium increased by 35%, 55%, 36% and 34%, respectively. This effect was blocked by Cap. Conclusion: Cap inhibits hypoxia-induced pulmonary artery smooth muscle cell proliferation and collagen synthesis, which may be related to the block of L-type calcium channel.