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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-110－8mol／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、10nmol／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、50μmol／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、MAPK活性终止ET-1的细胞内信号转导途径有关。
The cultured rabbit aortic vascular smooth muscle cells (VSMCs) were stimulated with endothelin (ET-1), nitric oxide (NO) precursor L-Arg and NO donor SIN- , The activity of mitogen-activated protein kinase (MAPK) and the activity of protein kinase C (PKC) in VSMC3H-TdR cells were measured by MTT assay and ET-1 + SIN- Transduction pathway. The results showed that: (1) ET-110-8mol / L alone, 3H-TdR incorporation, MAPK activity and PKC activity increased 5 times, 4 times and 3 times (P <0.01) Arg or SIN-1 stimulation had no significant effect on the above parameters; (2) The combination of ET-1 and L-Arg (2, 5 and 10nmol / L), 3H-TdR incorporation, MAPK activity and PKC activity were significantly lower than (3) ET-1 combined with SIN-1 (5, 10, 50μmol / L), 3H-TdR incorporation, MAPK activity and PKC activity were also significantly lower than that of ET- group. The results suggest that NO inhibits the proliferation of VSMC induced by ET-1, which is related to the inhibition of ET-1 activation of PKC by MAPK and the termination of the intracellular signal transduction pathway of ET-1 by NO.