摘要
为了研究梗死心肌成纤维细胞对血管紧张素Ⅱ的反应性 ,应用酶法分离、培养经卡托普利和洛沙坦干预后的成年大鼠梗死心肌成纤维细胞 ,检测在不同处理因素下 ,血管紧张素Ⅱ对培养的成纤维细胞的3H 胸腺嘧啶脱氧核苷、1 4C 尿嘧啶核苷和3H 脯氨酸掺入率的影响。结果发现 ,在相同浓度血管紧张素Ⅱ (10 7mol L)的作用下 ,对照组的成纤维细胞对上述三种底物的掺入率均显著高于假手术组 (P <0 .0 5 ) ;而卡托普利和洛沙坦两干预组分别与假手术组相比 ,均无显著性差异 (P >0 .0 5 )。血管紧张素Ⅱ的上述作用均不能被血管紧张素Ⅱ 1型受体阻滞剂洛沙坦完全阻断 ,但能被血管紧张素Ⅱ特异性拮抗剂 (1.8血管紧张素Ⅱ和血管紧张素抗肽 )完全阻断。结果提示 ,血管紧张素Ⅱ可直接作用于非梗死区心肌的成纤维细胞 ,促进成纤维细胞的DNA、RNA和蛋白质合成 ;介导血管紧张素Ⅱ对成纤维细胞作用除血管紧张素Ⅱ 1型受体外 ,还有其他因素参与。长期应用卡托普利可显著降低心肌梗死后心肌成纤维细胞对血管紧张素Ⅱ的反应性 。
Aim To investigate the responseness of the fibroblasts from the myocardium infarcted rats to angiotensinⅡ(AngⅡ). Methods With the tissue isolation, cell culture and the uptake rates of 3 H thymidine ( 3 H TdR), 14 C uridine ( 14 C UR) and 3 H proline ( 3 H Pro) representing syntheses of DNA,RNA and collagen protein of isolated fibroblasts (Fbs) from the heart of myocardial infarction (MI) rats and sham operated (SO) which were treated with losartan or captopril for 6 weeks, respectively. Results The uptake rates of 3 H TdR, 14 C UR and 3 H Pro of Fbs from MI group treated with losartan or captopril are not significantly different from those of the SO one, respectively. These effects of AngⅡon Fbs are abolished completely by 1.8 AngⅡand angiotensin antipeptide, but not completely by angiotensin receptor 1 antagonist, losartan. Conclusion The findings suggest that the responsiveness of Fbs to AngⅡ from MI rats treated with either losartan or captopril is significantly lower than that from that from the MI rats. AngⅡ acts on the Fbs from normal or hypertrophied myocardium via not only AT1 receptor, but also other mechanisms involving in the effects of AngⅡ to Fbs.
出处
《中国动脉硬化杂志》
CAS
CSCD
2002年第2期115-117,共3页
Chinese Journal of Arteriosclerosis
基金
国家自然科学基金 (3 92 70 3 15 )
