Inhibitory effects of captopril on hypoxia-induced proliferation and collagen synthesis in pulmonary vascular smooth muscle cells.

Zhongguo yao li xue bao = Acta pharmacologica Sinica Pub Date : 1999-04-01

J Shen, Y Xu

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Abstract

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 mumol.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 mumol.L-1.

Conclusion: Cap inhibited hypoxia-induced proliferation and collagen synthesis in VSMC.

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卡托普利对缺氧诱导的肺血管平滑肌细胞增殖及胶原合成的抑制作用。

目的:研究卡托普利(Cap)对缺氧诱导的血管平滑肌细胞(VSMC)增殖及胶原合成的影响。方法:从兔肺动脉分离VSMC。通过[3H]胸苷和[3H]脯氨酸的掺入、细胞数量和细胞内钙浓度([Ca2+]i)来评估培养的VSMC。结果:Cap - 1mumol预处理肺VSMC。L-1阻断了低氧诱导的[3H]脯氨酸和[3H]胸苷的细胞数量增加和掺入，与低氧对照相比，它们分别减少了25%、21%和36%。它还能抑制缺氧条件下细胞内Ca2+浓度的升高。添加硝苯地平抑制缺氧刺激的胶原蛋白、DNA合成和[Ca2+]i的增加。Bay-K-8644增加了肺VSMC细胞数量(35%)、DNA(55%)、胶原合成(36%)和[Ca2+]i(33%)，而Cap 1 mumol.L-1完全消除了这种作用。结论:Cap可抑制缺氧诱导的VSMC细胞增殖和胶原合成。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Zhongguo yao li xue bao = Acta pharmacologica Sinica

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