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卡托普利对缺氧诱导的肺动脉平滑肌细胞增殖和胶的合成的抑制作用
引用本文:申捷 徐毅. 卡托普利对缺氧诱导的肺动脉平滑肌细胞增殖和胶的合成的抑制作用[J]. 中国药理学报, 1999, 20(4): 349-352
作者姓名:申捷 徐毅
作者单位:[1]徐州市第一人民医院 [2]湖南医科大学心血管生理研究所
摘    要:

关 键 词:卡托普利 肺动脉 血管平滑肌 缺氧症 胶原

Inhibitory effects of captopril on hypoxia-induced proliferation and collagen synthesis in pulmonary vascular smooth muscle cells.
J Shen,Y Xu. Inhibitory effects of captopril on hypoxia-induced proliferation and collagen synthesis in pulmonary vascular smooth muscle cells.[J]. Acta Pharmacologica Sinica, 1999, 20(4): 349-352
Authors:J Shen  Y Xu
Affiliation:Department of ICU, First People's Hospital of Xuzhou, Xuzhou Medical College, China. hjp112@public.xz.js.cn
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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