摘要
目的 研究血管紧张素Ⅱ (AngⅡ )及其受体拮抗剂对培养的大鼠血管平滑肌细胞 (VSMC)迁移能力影响 ,以探讨AngⅡ介导高血压、动脉粥样硬化和血管成形术后再狭窄斑块形成的生物学机制。 方法 采用改良Boyden小室 ,对不同浓度AngⅡ及其AT1R、AT2 R拮抗剂作用下VSMC跨膜迁移细胞数进行评价。结果 AngⅡ在一定的浓度范围内 (10 -11～ 10 -7mol/L )可以剂量依赖性地刺激体外培养的大鼠VSMC发生迁移。迁移的VSMC数在AngⅡ浓度为 10 -7mol/L时达到峰值 ,更高浓度的AngⅡ (10 -6mol/L)干预VSMC后 ,VSMC迁移数量的增加幅度反而比较低浓度的AngⅡ作用时减小 (与 10 -7mol/LAngⅡ组比较 ,P <0 0 1)。AT1R拮抗剂CV 11974剂量依赖性抑制AngⅡ诱导VSMC跨膜迁移 ,AT2 R拮抗剂PD12 3319对此无影响。结论 AngⅡ在AT1R介导下发挥其影响VSMC迁移行为的生物学效应 ,较低浓度AngⅡ促进VSMC迁移 。
Objective To determine the effects of Angiotensin Ⅱ(AngⅡ) on migration of rat smooth muscle cells and investigate the role of Angiotensin Ⅱin the development of hypertension,atherosclerosis,and restenosis. Methods Migration of rat VSMCs was assayed by a modification of Boyden's chamber method in the presence different concentrations of AngⅡ , AT 1 receptor antagonist CV11974, and AT 2 receptor antagonist PD123319. Results AngⅡ increased migration activity in a concentration dependent manner from 10 -11 mol/L to 10 -7 mol/L. The maximal effect was observed at 10 -7 mol/L of AngⅡ. At a higher concentration of AngⅡ(10 -6 mol/L) cells migration was reduced( P <0 01 versus 10 -7 mol/L AngⅡ). AT 1 R antagonist CV11974 inhibited AngⅡ induced migration of VSMCs in a concentration dependent manner. AT 2 R antagonist PD123319 had no significant effect. Conclusion The effect of AngⅡ on rat VSMC migration is mediated by AT 1 receptor and in a concentration dependent manner. Lower concentration of AngⅡ stimulated VSMC migration and the effect is markedly weakened in higher concentration of AngⅡ.
出处
《高血压杂志》
CSCD
2001年第3期247-249,共3页
Chinese Journal of Hypertension
