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作 者:申景平[1] 雷立权 高广道 李瑞峰[1] 李炯 张庆殷[2]
机构地区:[1]山东医科大学病理生理教研室 [2]山东医科大学附属医院 [3]西安医科大学病理生理教研室
出 处:《中国病理生理杂志》1999年第1期5-7,共3页Chinese Journal of Pathophysiology
基 金:国家"八五"攻关和国家自然科学基金
摘 要:目的和方法:本实验利用酶法分离、培养成年大鼠心肌成纤维细胞(Fbs),观察了血管紧张素Ⅱ(AngⅡ)在不同处理因素下对Fbs的3H-TdR、14C-UR、3H-Pro掺入率的影响。结果:在相同浓度(107mol/L)AngⅡ作用下,MI组Fbs对上述3种标记底物的掺入率均显著高于假手术(SO)组(P<0.05)。AngⅡ的上述作用,可被特异性AngⅡ拮抗剂[18]AngⅡ和血管紧张素抗肽(Ang-AP)完全阻断,却不能被Losartan完全阻断。结论:AngⅡ可直接作用于心肌Fbs,促进Fbs的DNA、RNA和胶原蛋白的合成。MI组大鼠Fbs对AngⅡ反应性显著高于SO组,介导AngⅡ对Fbs的作用除AT1外。AIM and METHOD: Isotope-labelled substrate incorporation method was used to investigate the effect of angiotensin Ⅱ(Ang Ⅱ) on the syntheses of DNA, RNA and collagen protein of isolated fibroblasts(Fbs) from myocardial infarction (MI) and sham operated (SO) rats in different conditions. RESULTS: The incorporating rates of 3H-thymidine, 14 C-uridine and 3H-proline of Fbs from MI group were significantly higher than that of SO group, respectively. These effects of Ang Ⅱ on Fbs were abolished completely either by angiotensin antagonists, 1 8 Ang Ⅱ, or by angiotensin antipeptide. On the other hand,angiotensin receptor antagonist, losartan, can not thoroughly eliminate the above-mentioned effects of Ang Ⅱ. CONCLUSIONS: (1) Ang Ⅱ promoted the syntheses of DNA, RNA and collagen protein in Fbs; (2) The responsiveness of Fbs to Ang Ⅱ from MI rats was higher than that of normal rats; (3)AT 1 receptor is not the only substype which regulates the action of Ang Ⅱ to Fbs metabolism.
分 类 号:R542.220.2[医药卫生—心血管疾病]
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