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目的:观察血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)对血管平滑肌细胞(VSMC)血管紧张素Ⅱ受体1(AT1R)、血管紧张素Ⅱ受体2(AT2R)mRNA表达的影响。方法:人脐带动脉平滑肌细胞体外原代培养,AngⅡ干预后RT-PCR测定VSMC的AT1R、AT2R mRNA的表达,并观察AT1R阻滞剂氯沙坦、AT2R阻滞剂PD123319对AngⅡ上述诱导作用的影响。结果:1AngⅡ作用于VSMC后,AT1R mRNA表达增强(P<0.01),氯沙坦阻断AT1R后,AT1R mRNA表达显著下降(P<0.01),PD123319阻断AT2R后,AT1R mRNA表达无显著性变化;2AngⅡ作用于VSMC后,AT2R mRNA表达无显著性增强,氯沙坦及PD123319作用后,AT2R mRNA表达也未见显著性变化。结论:1AngⅡ可诱导VSMC AT1R mRNA表达,AT1R在此过程中起重要介导作用,AT1R阻滞剂氯沙坦可有效抑制AngⅡ的这种诱导作用;2相对于AT1R,AngⅡ不能诱导VSMC AT2R mRNA表达增加。所以推测AngⅡ差异化诱导VSMC AT1R、AT2R mRNA表达,导致AT1R、AT2R失衡。
Objective: To observe the effects of angiotensin Ⅱ (AngⅡ) on the mRNA expression of AT1R and AT2R in vascular smooth muscle cells (VSMCs). Methods: Human umbilical artery smooth muscle cells were primarily cultured in vitro. The expression of AT1R and AT2R mRNA in VSMCs was determined by RT-PCR after AngⅡ intervention. The effects of AT1R inhibitor losartan and AT2R inhibitor PD123319 on the above induction were observed . Results: AT1R mRNA expression was increased in VSMC treated with 1 ng / ml AngⅡ (P <0.01), AT1R mRNA was decreased significantly (P <0.01) after AT1R was blocked by losartan, but AT1R mRNA was not significantly changed after AT2R was blocked by PD123319 ; AT2R mRNA expression did not increase significantly after treated with 2AngⅡ in VSMC, and there was no significant change of AT2R mRNA expression after treated with losartan and PD123319. CONCLUSION: 1AngⅡinduced the expression of AT1R mRNA in VSMC. AT1R plays an important role in this process. Losartan, an AT1R inhibitor, can effectively inhibit this effect induced by AngⅡ.2 AngⅡ can not induce VSMC AT2R mRNA expression compared with AT1R increase. Therefore, it is hypothesized that the AngⅡdifferentiation induces the expression of AT1R and AT2R mRNA in VSMC, resulting in imbalance of AT1R and AT2R.