摘要
目的 :探讨血管紧张素Ⅱ (AngⅡ )对成年大鼠心肌成纤维细胞 (MFs)分泌内皮素 - 1(ET - 1)、一氧化氮 (NO)的影响。方法 :采用酶消化法和差速贴壁分离法获取MFs ,应用放射免疫分析法、硝酸还原酶法分别测定不同条件下培养的第二代心肌MFs培养液中的ET - 1、NO水平。结果 :一定浓度范围内的AngⅡ可按剂量依赖方式促MFs分泌ET - 1,血管紧张素Ⅱ 1型受体 (AT1R)拮抗剂losartan可阻断AngⅡ的上述作用 ;AngⅡ可抑制心肌MFs分泌NO ,加losartan后再加AngⅡ培养发现 ,MFs分泌NO能力不但不降低 ,而且还高于对照组 (P <0 0 1)。结论 :AngⅡ可通过AT1R促成年大鼠心肌MFs分泌ET - 1,主要通过AT1R影响MFs分泌NO ,从而改变ET - 1/NO比值。AngⅡ可能通过影响MFs分泌的生物活性物质网络平衡关系改变 ,发挥其促心肌肥厚及心力衰竭效应。
AIM: To investigate the effects of AngⅡon the production of ET-1, NO from myocardial fibroblasts (MFs) of adult rat. METHODS: MFs were extracted by enzymatic digestion and anchorage velocity-dependent separation method. In this study, the changes of ET-1 and NO production from MFs in the second passage were examined by radioimmunoassay and by nitrate reductase-dependent assay, separatively. RESULTS: In a specific concentration range, AngⅡ increased ET-1 synthesis in MFs in a concentration-dependent manner. Losartan, the antagonist of angiotensin Ⅱ 1 type recepters (AT 1R), blocked the above effects. AngⅡ may inhibit NO synthesis in MFs. When MFs were treated with losartan+AngⅡ, the production of NO increased significantly, and was higher than that treated with the others( P< 0.01). CONCLUSION: AngⅡ may increase the production of ET-1 in MFs via AT 1R and affect NO production in MFs mainly via AT 1R to change the ratio of ET-1 and NO. AngⅡ maybe exert inductive effects on myocardial hypertrophy and heart failure by affecting these complicated balances between bioactive factors produced from MFs.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第9期1050-1052,共3页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目(No.39570309)
