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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 )?