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作 者:张琪[1] 丁金凤[1] 赵秀文[1] 任兵[1] 刘冬青[1]
机构地区:[1]中国医学科学院中国协和医科大学心血管病研究所,中国医学科学院中国协和医科大学阜外心血管病医院
出 处:《中国循环杂志》1995年第4期219-221,共3页Chinese Circulation Journal
基 金:"八五"国家科技攻关资助
摘 要:为研究卡托普利(CAP)对心血管组织肾素─血管紧张素系统的影响,5周龄雄性卒中型自发性高血压大鼠(SHRsp)随机分为实验组(n=12)及对照组(n=8),分别于食管内喂饲CAP(60mg·kg-1/d)或蒸馏水,每日1次,持续8周。用放射免疫法测定血浆肾素活性、血管紧张素Ⅱ(AngⅡ),心肌和主动脉平滑肌(ASM)的肾素浓度(RC)和AngⅡ含量。结果显示,实验组血压不升高,心室重/体重比值也低于对照组;心肌和ASM的RC比对照组高;而AngⅡ被明显抑制,分别为7.02±0.96比13.40±5.39(P<0.01)和24.80±4.93比33.65±8.89pg/mg蛋白(P<0.02)。这说明,CAP长期治疗可明显阻止SHRsp的血压上升及心肌肥厚的发生,降低心肌和ASM中AngⅡ含量,提示在这种模型,CAP降压及抗心肌肥厚的重要机制之一是阻断心血管组织局部AngⅡ的生成。To study the effect of chronic angiotensin converting enzyme(ACE) inhibition on cardiovascular renin-angiotensin system(RAS), captopril(CAP, 60mg. kg-1/day, n=12) and vehicle(n=8) were given to 5-week old male stroke-prone spontaneously hypertensive rats(SHRsp) by gavage for 8 weeks as experimental(CAP) and control(C) groups, respectively.Plasma renin activity(PRA) and angiotensin II(Ang II) , ventricular and aortic smooth muscle(ASM) renin concentration(RC) and Ang II were measured by radioimmunoassay. The results showed that in the CAP group, hypertension was not developed, ratio of ventricular to body weight was lower and tissue RC was higher than the C group; Ang II in the ventricular myocardium and ASM were significantly suppressed(7.02±0.96 vs. 13. 40±5. 39 pg/mg pr, P<0.01 and 24. 80±4. 93 vs. 33. 65±8. 89 pg/mg pr. P<0. 02 , respectively) without inhibition of plasma Ang II. The results of the hypotensive and anti-myocardio-hypertrophic effects by chronic ACE administration together with the decrease of Ang II in the myocardium and ASM suggest that the suppression of myocardial and vascular smooth muscle Ang II formation is one of the important mechanisms in the anti-hypertensive and anti-myocardio-hypertrophic actions of CAP.
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