摘要
以培养的自发性高血压大鼠（SHR）和正常血压（WKY）大鼠主动脉平滑肌细胞（ASMC）为模型,采用Northern印迹和逆转录-聚合酶链式反应（RT-PCR）技术分别检测ASMC中血管紧张素原（Ang N）和血管紧张素Ⅱ（Ang Ⅱ）的AT_1型受体的基因表达,并用紫外法和放射免疫法分别测定培养液中的血管紧张素Ⅰ转换酶（ACE）活性和AngⅡ的含量。结果表明,基础状态及给予外源性碱性成纤维细胞生长因子（bFGF,10 ng/ml）刺激后,SHR的ASMC中上述4种实验参数的水平均明显高于WKY大鼠。提示SHR ASMC中的肾素—血管紧张素系统（RAS）处于高功能状态;bFGF能促进Ang N基因表达、激活ACE,进而导致Ang Ⅱ生成增加,同时它对AT_1受体基因表达也有调节作用,bFGF的上述作用可能是高血压时血管RAS高功能状态发生和维持的一个重要机制。
The purpose of this study is to explore mechanisms by which vascular renin-angiotensin system (RAS ) is activited in spontaneously hypertensive rats ( SHR ). Angiotensin Ⅰ converting enzyme(ACE) activity and angiotensin Ⅱ ( Ang Ⅱ) content in the media of cultured aortic smooth muscle cells (ASMC) from SHR and Wistar-Kyoto (WKY) rats were measured by colorimetry and radioim-munoassay, respectively. The expression of an-giotensinogen (Ang N) mRNA and Ang Ⅱ type Ⅰ (AT1) receptor mRNA of ASMC from both strains were detected by Northern blot and reverse transcrip-tion-polymerase chain reaction (RT-PCR), respectively. Our results demonstrated that, basic fibrob-last growth factor ( bFGF, 10 ng/ml) significantly promoted the expression of Ang N mRNA, activated ACE activity and stimulated the release of Ang Ⅱ from ASMC in both strains. Furthermore, bFGF(10 ng/ml) obviously enhanced the expression of AT, receptor mRNA. Both in basal and in bFGF-stimulated states, levels of the above-mentioned four experimental parameters in SHR were higher than those in WKY rats. These results indicate that RAS activities are increased in cultured ASMC from SHR, and bFGF might be an important endogenous activator of enhanced vascular RAS activity in SHR.
出处
《高血压杂志》
CSCD
1995年第4期255-259,共5页
Chinese Journal of Hypertension
基金
国家"八五"科技攻关课题(85-915-03-02)
关键词
碱性成纤维细胞
生长因子
肾素
RAS
高血压
vascular renin-angiotensin system
basic fibroblast growth factor
hypertension
