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| KATP通道开放剂吡那地尔对兔肺动脉平滑肌细胞增殖的影响 | |
| 引用本文： | 解卫平,丁建花,王虹,汪海,胡刚.KATP通道开放剂吡那地尔对兔肺动脉平滑肌细胞增殖的影响[J].中国临床药理学与治疗学,2005,10(1):20-23. |
| 作者姓名： | 解卫平 丁建花 王虹 汪海 胡刚 |
| 作者单位： | 1. 南京医科大学药理学系,南京,210029,江苏;南京医科大学第一附属医院呼吸内科,南京,210029,江苏 2. 南京医科大学药理学系,南京,210029,江苏 3. 军事医学科学院药物毒物研究所,北京,100850 |
| 基金项目： | 国家创新药物基础研究重大项目基金 (№ 9690 10 10 1)，国家自然科学基金 (№ 3 9970 846)，江苏省科委社会发展基金 (№BJ2 0 0 0 0 5 1)，江苏省教育厅基金 (№ 0 0KJB3 2 0 0 0 9) |
| 摘 要： | 目的 :研究吡那地尔 (pinacidil,Pin)对内皮素 1(ET 1)诱导培养的兔肺动脉平滑肌细胞 (PASMC)增殖的影响。方法 :内皮素 1刺激培养兔PASMC增殖模型 ;以氚 胸腺嘧啶核苷 (3 H] TdR)掺入法观察细胞增殖及脱氧核糖核苷酸 (DNA)合成 ;流式细胞仪技术检测兔PASMC细胞周期。结果 :吡那地尔可剂量依赖性的抑制内皮素 1所致的 3 H] TdR掺入量增多 ,阻止兔PASMC由静止期 (G0 G1期 )进入DNA合成期 (S期 )和有丝分裂期 (G2 M期 )。ATP敏感性钾通道 (KATP)阻断剂格列本脲可拮抗吡那地尔对 3 H] TdR掺入的抑制作用。结论 :吡那地尔可能通过激活KATP通道抑制内皮素 1诱导兔肺动脉平滑肌细胞的增殖 ,可望用于治疗肺动脉高压时所致的肺动脉重构。 |
| 关 键 词： | 吡那地尔 肺动脉平滑肌细胞 内皮素-1 ATP敏感性钾通道 |
| 文章编号： | 1009-2501(2005)01-0020-04 |
| 修稿时间： | 2004年12月8日 |
Effects of pinacidil on proliferation of cultured rabbit pulmonary arterial smooth muscle cells induced by endothelin-1 |
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| XIE Wei ping ,DING Jian hua ,WANG Hong ,WANG Hai ,HU Gang.Effects of pinacidil on proliferation of cultured rabbit pulmonary arterial smooth muscle cells induced by endothelin-1[J].Chinese Journal of Clinical Pharmacology and Therapeutics,2005,10(1):20-23. | |
| Authors: | XIE Wei ping DING Jian hua WANG Hong WANG Hai HU Gang |
| Institution: | XIE Wei ping 1,2,DING Jian hua 1,WANG Hong 1,2,WANG Hai 3,HU Gang 1 1 Department of Pharmacology,2 Department of pulmonology,the First Affiliated Hospital,Nanjing Medical University,Nanjing 210029,Jiangsu,China, 3 Institute of Pharmacology and Toxicology,Molitary Medicine and Science Academic,Beijing 100850,China |
| Abstract: | AIM : To explore the effects of pinacidil on the proliferation of rabbit pulmonary arterial smooth muscle cell (PASMC) induced by endothelin 1 in vitro . METHODS : The experimental model of proliferation of rabbit pulmonary arterial smooth muscle cell (PASMC) induced by endothelin 1 in vitro was established and 3H] thymidine ( 3H] TdR) incorporation and flow cytometric analysis (FCA) were used. Z RESULTS : Pinacidil markedly inhibited 3H] TdR incorporation of PASMC induced by ET 1 and held back PASMC from static phase (G 0/G 1) to DNA synthesis (S) and mitotic phase (G 2/M) in the dose dependent manner. Glibenclimide blocked the effects of pinacidil on 3H] TdR incorporation. CONCLUSION : Pinacidil has an inhibitive effect on PASMC proliferation induced by ET 1 through activating ATP sensitive potassium (K ATP ) channels and K ATP channels might play an important pathophysiologic role in the vascular remodeling. Pinacidil is a promising candidate in the treatment of pulmonary hypertension. |
| Keywords: | pinacidil pulmonary arterial smooth muscle cell endothelin-1 ATP sensitive potassium channels |
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