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目的:研究局部血管紧张素转化酶及血管紧张素Ⅱ和低氧促进肺动脉平滑肌细胞增殖作用之间的关系。方法:分离培养肺内小动脉平滑肌细胞,测定[~3H]thymidine掺入和细胞计数作为细胞增殖的指标。结果:低氧显著促进培养的肺内小动脉平滑肌细胞增殖,其[~3H]thymidine掺入和细胞计数分别增加166.6％(P<0.01)和52.0％(P<0.01)。captopril和losartan预处理可显著抑制低氧对肺内小动脉平滑肌细胞增殖的促进作用,[~3H]thymidine掺入分别被抑制51.3％(P<0.01)和49.8％(P<0.01),细胞计数分别被抑制22.2％(P<0.01)和17.9％(P<0.01)。而PD-123319基本无明显作用。结论:肺内小动脉平滑肌细胞局部血管紧张素转化酶的过度表达及血管紧张素Ⅱ在低氧促平滑肌细胞增殖中发挥重要作用。
Objective: To investigate the relationship between local angiotensin converting enzyme and angiotensin Ⅱ and hypoxia in promoting proliferation of pulmonary artery smooth muscle cells. Methods: Pulmonary arteriolar smooth muscle cells were isolated and cultured. The [~ 3H] thymidine incorporation and cell count were measured as indicators of cell proliferation. RESULTS: Hypoxia significantly promoted the proliferation of VSMCs. The [~ 3H] thymidine incorporation and cell counts increased by 166.6% (P <0.01) and 52.0% (P <0.01), respectively. Pretreatment with captopril and losartan significantly inhibited hypoxia-induced pulmonary artery smooth muscle cell proliferation in a dose-dependent manner. [~ 3H] thymidine incorporation was inhibited by 51.3% (P <0.01) and 49.8% (P <0.01) Were inhibited by 22.2% (P <0.01) and 17.9% (P <0.01), respectively. The PD-123319 basically no significant effect. Conclusion: The overexpression of local angiotensin converting enzyme in pulmonary arteriolar smooth muscle cells and angiotensin Ⅱ play an important role in the hypoxia - induced smooth muscle cell proliferation.