摘要
目的 观察血管紧张素Ⅱ (AngⅡ )AT1受体拮抗剂缬沙坦和盐皮质激素受体拮抗剂螺内酯对自发性高血压大鼠(SHR)主动脉生长因子和Ⅰ型胶原的影响。方法 将 18只雄性SHR随机分为三组 :SHR阳性对照组、缬沙坦治疗组、螺内酯治疗组 ,每组 6只 ;两治疗组分别用缬沙坦 3 0mg·kg-1·d-1、螺内酯 2 0mg·kg-1·d-1溶于饮水灌胃 ,1次 /d ,连续治疗 13周 ;两对照组给正常饮水。鼠尾法测大鼠尾动脉收缩压。用RT -PCR方法检测大鼠主动脉TGFβ1、HGF、Ⅰ型胶原mRNA水平。结果 治疗 13周后缬沙坦组和螺内酯组TGFβ1、Ⅰ型胶原mRNA水平组明显低于SHR对照组 ( P <0 0 1) ,但较WKY组有所升高 ( P <0 0 1)。SHR对照组的HGFmRNA水平低于WKY组 (P <0 0 1) ,缬沙坦组和螺内酯组的HGFmRNA水平高于SHR对照组 (P <0 0 1,P <0 0 5 ) ,低于WKY组 (P <0 0 1)。结论 AngⅡAT1受体拮抗剂缬沙坦和盐皮质激素受体拮抗剂螺内酯均能抑制SHR的血管纤维化 ,在药物干预的过程中同时伴HGFmRNA水平升高。
Objective To observe the effects of angiotensin Ⅱ(AngⅡ) AT 1 receptor antagonist,valsartan and mineralocorticoid receptor antagonist,spironolactone on growth factors and type Ⅰ collagen in aorta in spontaneously hypertensive rat(SHR).Methods Six-week male SHRs were divided into three groups at random:SHR control group,valsartan group and spironolactone group;six homogenous Wistar Kyoto(WKY) rats was served as normal control group.Valsartan 30mg·kg -1 ·d -1 ,spironolactone 20mg·kg -1 ·d -1 were respectively administered to rats in valsartan group and spironolactone group.Expressions of transforming growth factor β 1(TGF β 1),hepatocyte growth factor(HGF) and type Ⅰ collagen gene mRNA in aorta were determined by RT-PCR.Results Compared with those of untreated SHR group,levels of TGFβ1 and type Ⅰ collagen gene mRNA expression in aortas treated with valsartan and spironolactone for 13 weeks were significantly reduced(P<0 01,respectively),but higher than those in WKY group.Level of HGF mRNA expression in aortas of untreated SHR group were obviously lower than those of WKY group(P<0 01).Compared with those of untreated SHR group,levels of HGF mRNA expression in aortas treated with valsartan and spironolactone were significantly increased(P<0 01,P<0 05,respectively).Conclusions These results indicated that Ang Ⅱ AT 1 receptor antagonist and mineralocorticoid receptor antagonist could prevent vascular fibrosis,a significant increase of HGF mRNA in aorta in process of drug treatment HGF could play an important role in preventing vascular remodeling through its antifibrosis action.
出处
《中国医师杂志》
CAS
2003年第7期874-876,共3页
Journal of Chinese Physician
基金
湖北省教育厅自然基金资助项目 (30 1 1 4 0 0 80 )
