血管紧张素Ⅱ促进培养的肺内小动脉平滑肌细胞增殖作用及其机制

目的 :探讨血管紧张素Ⅱ (AngⅡ )促培养的肺内小动脉平滑肌细胞增殖作用机制。方法 :采用培养的肺内小动脉平滑肌细胞 (PASMCs)观察外源性AngⅡ对PASMCs增殖的影响及机制。结果 :外源性AngⅡ显著促进培养的PASMCs的增殖 ,在 10 - 1 0 ～ 10 - 5mol·L- 1 呈剂量依赖性。钙拮剂Verapamil,PKC抑制剂Staurosporine和Na+ K+ 交换抑制剂amiloride能显著抑制AngⅡ促进PASMC增殖的作用 ,3H Tdr掺入率和细胞记数分别下降 4 4 .3% ,33.2 % ,36 .5 %和31.7% ,2 5 .5 % ,2 8.1%。结论 :AngⅡ显著促进培养的PASMCs增殖 ;Ca2 + ,PKC和Na+ K+ ATPase的激活 ,可能是AngⅡ促PASMCs增殖的重要细胞内信号传导机制。

Proliferative effect of angiotensin Ⅱ on cultured PASMCs and its mechanisms

Objective To study the effect of exogenous angiotensin Ⅱ (Ang Ⅱ) on the proliferation of cultured pulmonary artery smooth muscle cells (PASMCs) and its mechanisms. Methods We adopted cultured PASMCs to observe the effect of exogenous AngⅡ on the proliferation of cultured PASMCs and its mechanisms.Results Exogenous AngⅡ stimulated the proliferation of cultured PASMCs in a dose dependent manner (10 -10 ～10 -5 mol·L -1 ). The proliferative effect of AngⅡ on PASMCs was markedly inhibited by calcium channel antagonist Verapamil, PKC inhibitor Staurosporine and Na + K + ATPase inhibitor amiloride; the decrease rates in 3 H Tdr incorporation and cell numbers were 44.3%, 33.2%, 36.5% and 31.7%, 25.5%, 28.1%, respectively (P<0.01). Conclusion AngⅡ significantly stimulates the proliferation of cultured PASMCs, and the activation of Ca 2+ channel, PKC and Na + K + ATPase may be important intracellular signal transduction mechanisms.