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目的以20周龄自发性高血压大鼠(SHR)和正常血压大鼠(WKY)胸主动脉平滑肌细胞(ASMC)为模型,探讨SHRASMC异常增殖和自身肾素-血管紧张素系统(RAS)的关系。方法用3H-TdR参入量和倍增时间(DT)反映ASMC的增殖能力,放射免疫法测定血管紧张素Ⅱ(AngⅡ)浓度,紫外分光光度法测定血管紧张素转换酶(ACE)活性。结果(1)SHRASMC3H-TdR参入量显著高于WKY,DT显著短于WKY(P<0.01)。基础状态下,SHRASMC合成AngⅡ、ACE以及分泌AngⅡ的量显著高于WKY(P<0.01)。(2)在含2%FCS的培养基中,10-6mol/LAngⅡ使SHR、WKY的3H-TdR参入量分别提高到对照组的3.3倍、2.2倍(P<0.01),SHRASMC在不同浓度AngⅡ刺激时的3H-TdR参入量显著高于WKY(P<0.01),10-6mol/LAngⅡ使SHRASMC细胞数增加72.5±23.1%(P<0.01),WKYASMC细胞数无显著增加,10倍浓度AngⅡ的Saralasin对SHR、WKY3H-TdR参入的抑制率分别为66.7±3.3%,44.7±9.9%(P<0.01)?
Objective To investigate the effects of SHRASMC on the proliferation of aortic smooth muscle cells (ASMCs) in spontaneously hypertensive rats (SHR) and normotensive rats (WKY) at 20 weeks of age and to explore the relationship between the abnormal proliferation of SHRASMC and the renin-angiotensin system relationship. Methods 3H-TdR incorporation and DT were used to reflect the proliferation of ASMC. Angiotensin Ⅱ (AngⅡ) concentration was measured by radioimmunoassay. The activity of angiotensin converting enzyme (ACE) was measured by ultraviolet spectrophotometry. Results (1) SHRASMC3H-TdR incorporation was significantly higher than WKY, DT was significantly shorter than WKY (P <0.01). Under basic conditions, the amounts of AngⅡ, ACE and AngⅡ secreted by SHRASMC were significantly higher than those of WKY (P <0.01). (2) In the medium containing 2% FCS, the 3H-TdR incorporation of SHR and WKY increased to 3.3 and 2.2 times (P <0.01) , SHRASMC incorporation of 3H-TdR was significantly higher than that of WKY (P <0.01) when AngⅡ was stimulated with different concentration, and the number of SHRASMC increased by 72.5 ± 23.1% (P <0.01) with 10-6mol / ), No significant increase in WKYASMC cell number, Saralasin 10 times the Ang Ⅱ concentration of SHR, WKY3H-TdR accession inhibition rates were 66.7 ± 3.3%, 44.7 ± 9.9% (P <0.01 )?