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INHIBITION OF SIGNAL TRANSDUCTION PATHWAYS OF ENDOTHELIN-1-INDUCED PROLIFERATION OF VASCULAR SMOOTH MUSCLE CELLS BY NITRIC OXIDE
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- Author:
- No author available
- Journal Title:
- ACTA PHYSIOLOGICA SINICA
- Issue:
- 4
- DOI:
- 10.3321/j.issn:0371-0874.1998.04.004
- Key Word:
- 一氧化氮;内皮素;丝裂素活化蛋白激酶;蛋白激酶C;血管平滑肌细胞;细胞增殖
Abstract： 培养的家兔胸主动脉血管平滑肌细胞(VSMC)分别以内皮素(ET-1)、一氧化氮(NO)前体L-Arg和NO供体SIN-1刺激,或用ET-1+L-Arg、ET-1+SIN-1联合刺激,测VSMC3H-TdR掺入、丝裂素活化蛋白激酶(MAPK)活性及蛋白激酶C(PKC)活性的改变,以研究NO抑制ET-1促VSMC增殖作用的信号转导途径.结果表明:(1) ET-1 10-8 mol/L单独刺激,3H-TdR掺入、MAPK活性、PKC活性分别较对照组增加5倍、4倍和3倍(P＜0.01);L-Arg或SIN-1刺激对上述指标无明显影响;(2)ET-1与L-Arg(2、5、10 mmol/L)联合刺激,3H-TdR掺入、MAPK活性和PKC活性均明显低于ET-1单独刺激组;(3)ET-1与SIN-1(5、10、50 μmol/L)联合刺激,3H-TdR掺入、MAPK活性和PKC活性也均明显低于ET-1单独刺激组.结果提示:NO抑制ET-1促VSMC增殖的作用,此作用与NO抑制ET-1激活PKC、APK活性终止ET-1的细胞内信号转导途径有关.
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