血管紧张素Ⅱ刺激肥大心肌细胞和心肌成纤维细胞核酸蛋白质及胶原合成  

Angiotensin Ⅱ stimulates the syntheses of DNA,RNA,protein and collagen in isolated cardiomyocytes and cultured cardiac fibroblasts from hypertrophied rat heart

作　　者：田斌[1] 高广道[1] 曹治平[1] 卢兴[1] 

机构地区：[1]西安医科大学病理生理教研室,北京医科大学第三临床医学院血管医学研究所

出　　处：《中国病理生理杂志》1995年第5期450-454,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金;"八五"攻关资助

摘　　要：本实验用压力（ＰＯ）和容量超负荷（ＶＯ）性分离的肥大心肌细胞（ＭＣ）及培养的心肌成纤维细胞（Ｆｂｓ），就血管紧张素（Ａｎｇ）Ⅱ对其￣３Ｈ－Ｌｅｕ，￣１４Ｃ－ＵＲ，￣３Ｈ－ＴｄＲ和￣３Ｈ－ｐｔｏ掺入率的影响进行了对比研究。发现尽管ＡｎｇⅡ可提高正常和两种肥大ＭＣ的￣３Ｈ－Ｌｅｕ和￣１４Ｃ－ＵＲ掺入率，但肥大ＭＣ增加幅度显著高于假手术对照（ＳＯ）组，尤其以ＶＯ组最为明显（Ｐ＜０．０５ｖｓＰＯ）。相反，ＰＯ组ＦｂＳ的￣３Ｈ－ＴｄＲ，￣１４Ｃ－ＵＲ和￣３Ｈ－Ｐｒｏ掺入率增加幅度又显著高于ＳＯ和ＶＯ组。除￣３Ｈ－Ｐｔｏ外，ＶＯ组的￣３Ｈ－ＴｄＲ及￣１４Ｃ－ＵＲ掺入率与ＳＯ组相比差异无显著性。表明ＡｎｇⅡ对两种肥大心肌的ＭＣ和Ｆｂｓ的核酸、蛋白质及胶原合成的促进作用存在明显差异。提示：ＡｎｇⅡ的这种作用可能是导致压力和容量超负荷性心肌肥大时，心肌实质细胞与胶原增生出现不同步发展的主要和直接原因之一。The effect of angiotensin( Ang)Ⅱ on the incorporation of￣3H-Leu,￣14C-UR,￣3H-TdR and￣3H-pro in isolated myocytes(MC)and cultured cardiac fibroblasts(Fbs )from pressure and volume overload(PO and VO)and normal rat hearts wasdetermined.It was shown that in spite of the increase of incorporation of￣3H-Leu and￣14C-UR either in normal or hypertrophied MC under the stimulation of Ang Ⅱ,theincrease rate of the incorporation in hypertrophied MC was much higher than that ofcontrols.The increase rate in MC of VO group was the highest one among the threegroups, whereas the increase rate of the incorporation of￣3H-TdR,￣14C-UR and ￣3H-pro inFbs of PO rats wa s much higher than those of Fbs from VO or SO rats.Except for￣3H-Pro,no significant differences in the incorporation of￣3H-TdR and￣14C-UR in Fbsbetween VO and SO groups.These findings indicated that there was obyious differencesin the syntheses of nucleotide,protein and collagen in MC and Fbs between tbe twomyocardial hypertrophy models under the stimulation of AngⅡ,These differences maybe one of the main and direct cause for the heterogeneous process of myocardial hyper-trophy and hyperplasia of heart collagen during pressure and volume overload.

关 键 词：血管紧张素 成纤维细胞 核酸 蛋白质 心肌肥大 

分 类 号：R542.202[医药卫生—心血管疾病]