自发性高血压大鼠高血压形成前期血管平滑肌细胞增殖和肾素-血管紧张素系统的关系  

The relationship between proliferation of vascular smooth muscle cells and the renin angiotensin system in prehypertensive phase of SHR

作　　者：王向宇[1,2] 吴可贵[1,2] 张更 晋学庆[1,2] 王华军[1,2] 

机构地区：[1]福建医学院附属第一医院高血压研究室 [2]福建医学院解剖研究室

出　　处：《中华心血管病杂志》1997年第3期225-228,共4页Chinese Journal of Cardiology

基　　金：福建省自然科学基金

摘　　要：通过体外培养３周龄自发性高血压大鼠（ＳＨＲ）胸主动脉血管平滑肌细胞（ＡＳＭＣ），探讨ＳＨＲ高血压形成前期ＡＳＭＣ是否存在异常增殖，以及与循环、血管局部血管紧张素Ⅱ（ＡｎｇⅡ）、血管紧张素转换酶（ＡＣＥ）的关系。结果表明：３周龄ＳＨＲＡＳＭＣ肾素－血管紧张素系统（ＲＡＳ）处于高功能状态，合成ＡｎｇⅡ、ＡＣＥ，分泌ＡｎｇⅡ的量比ＷＫＹ高（Ｐ＜０．０５），并呈现异常增殖，３Ｈ－ＴｄＲ参入增加，倍增时间（ＤＴ）缩短（Ｐ＜０．０１）。血管紧张素转换酶抑制剂（ＡＣＥＩ）卡托普利、ＡｎｇⅡ受体拮抗剂Ｓａｒａｌａｓｉｎ长期干预可通过抑制ＳＨＲＡＳＭＣＡｎｇⅡ生成或阻断ＡｎｇⅡ的作用进而抑制其异常增殖。而ＷＫＹ血浆ＡｎｇⅡ、ＡＣＥ活性反比ＳＨＲ高（Ｐ＜０．０１）。说明：血管局部ＲＡＳ处于高功能状态对ＳＨＲ高血压前期ＡＳＭＣ异常增殖起重要作用，而循环ＲＡＳ则不起作用。The purpose of the study was to explore whether the cultured aortic smooth muscle cells(ASMC) proliferates abnormally and whether there was any relationship between ASMC proliferation and circulating or vascular angiotensin II(Ang Ⅱ), angiotension converting enzyme (ACE) activities in prehypertensive phase of SHR. Using 3-week-old SHR and WKY for experiments, the data revealed that SHR ASMC renin angiotensin system (RAS) is activated. The level of Ang Ⅱ ACE at SHR ASMC synthesized and secreted was much higher than that of KWY ( P <0 05). SHR ASMC proliferated abnormally 3H TdR incorporation of SHR ASMC was obviously higher in SHR compared with WKY and the doubling time (DT) was shorter comopared with WKY ( P <0.01). Enhanced proliferation of SHR ASMC could be inhibited by long term intervention of angiotension converting enzyme inhubitor (ACEI) captopril and Ang Ⅱ receptor antagonist saralasin. However the level of plasmic Ang Ⅱ, ACE activities were lower in SHR compared with WKY ( P <0 01). Conclusion: the hyperreactivity of vascular RAS, not circulating RAS may play an important role in SHR ASMC abnormal proliferation in prehypertensive phase.

关 键 词：高血压 血管平滑肌 血管紧张素 

分 类 号：R544.102[医药卫生—心血管疾病]