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血管紧张素在培养乳鼠心肌细胞肥大发生中的作用

Effect of angiotensin on the hypertrophy of myocardial cells in culture

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【作者】 田斌卢兴陈雁群程薇

【Author】 Tian Bing, Lu Xin, et al Department of pathophysiolgy, Xian Medical University, Xiam

【机构】 西安医科大学病理生理教研室西安医科大学病理生理教研室

【摘要】 本实验观察到血管紧张素Ⅰ、Ⅱ(AngⅠ、AngⅡ)均可促进培养的乳鼠心肌细胞(MC)DNA、RNA和蛋白质的合成。并发现随着AngⅠ和AngⅡ作用时间的延长,对MC的RNA和蛋白质合成的促进作用也逐渐增强,而对其DNA合成的促进作用则有一定的时间界限。此外,还发现在AngⅠ和AngⅡ长期作用下可使MC体积增大。当AngⅠ和血管紧张素转换酶(ACE)抑制剂同时加入培养基,则无上述结果发生。这提示血管紧张素可能在心肌肥大的发生中起一定作用,而且AngⅠ是通过MC本身的ACE将其转化为AngⅡ后才起作用的。

【Abstract】 Experiments were carried on cultured neonatal myocardial cells of rat to study the effects of angiotensin Ⅰ(AngⅠ) and Ⅱ (AngⅡ) on the synthesis of DNA, RNA, protein and on the cardiac hypertrophy. It was shown that the incorporation of both 3H-TdR and 14C-uR increased over a set of time periods after addition of AngⅠ and AngⅡ to the medium. The mean protein content of the single myocardial cell was also enhanced, and the volume of myocardial cell was increased significantly after a continuous stimulation of AngⅠ and AngⅡ for 7 days. No stimulation effect was observed either in the synthesis of DNA, RNA, and protein or in the volume of myocardial cells after addition of AngⅠ together with the angiotensin converting enzyme inhibitor(ACEI, captopril). These results indicated that: (1). AngⅠ acts as a regulator by its indirect stimulation effect on the synthesis of DNA, RNA and protein of myocardial cells, since it must be changed into AngⅡ by the ACE present in myocardial cells. The ACE can be inhibited by the ACEI: (2) The hypertrophy of cultured neonatal myocardial cells may induced by a continuous stimulation of AngⅠ and AngⅡ.

【关键词】 血管紧张素心肌肥大
【Key words】 AngiotensinMyocardiumHypertrophy
  • 【文献出处】 中国病理生理杂志 ,Chinese Journal of Pathophysiology , 编辑部邮箱 ,1992年01期
  • 【被引频次】14
  • 【下载频次】51
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