摘要
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 study the effect of captopril (Cap) on hypoxia-induced proliferation and collagen synthesis in vascular smooth muscle cells (VSMC). METHODS: VSMC were isolated from rabbit pulmonary artery. Cultured VSMC were evaluated by incorporation of [3H]thymidine and [3H]proline, cell number, and intracellular calcium concentration ([ Ca2 + ]i ). RESULTS: Pretreatment of pulmonary VSMC with Cap 1 μmol·L-1 blocked hypoxia-induced increase in cell number and incorporation of [3H]proline and [3H]thymidine, which were decreased 25 %, 21 %, and 36 % , respectively, as compared with hypoxic control. It also inhibited the increase of intracellular Ca2 + concentration under hypoxic condition. Addition of nifedipine inhibited hypoxia-stimulated increase in the collagen, DNA synthesis, and [Ca2+ ]i. Bay-K-8644 increased cell number (35 % ), DNA (55 % ), collagen synthesis (36 %), and [Ca2+ ]i(33 % ) in pulmonary VSMC, that was completely abolished by Cap 1 μmol·L-1. CONCLUSION: Cap inhibited hypoxia-induced proliferation and collagen synthesis in VSMC.
出处
《中国药理学报》
CSCD
1999年第4期349-352,共4页
Acta Pharmacologica Sinica
关键词
卡托普利
肺动脉
血管平滑肌
缺氧症
胶原
captopril
pulmonary artery
vascular smooth muscle
anoxia
cell division
collagen
calcium channels
