激肽系统在实验性糖尿病肾病发展中的作用研究  

The role of kinin-system in development-of diabetic nephropathy

作　　者：姚合斌[1] 潘长玉[1] 陆思珍[1] 郭爱岩[1] 汪寅章[1] 

机构地区：[1]中国人民解放军总医院内分泌科

出　　处：《中国糖尿病杂志》2000年第6期356-359,共4页Chinese Journal of Diabetes

摘　　要：目的观察激肽系统与糖尿病肾病的关系。方法用比色法测定激肽释放酶（ＴＫＡ）活性，用ＨＯＥ１４０和胰激肽释放酶改变激肽系统的功能。结果１８周时糖尿病组ＴＫＡ活性明显低于８周时的水平（Ｐ＜０．０１），与正常对照组比较有极显著差异（Ｐ＜０．０００１）。胰激肽释放酶治疗组ＴＫＡ活性升高（Ｐ＜０．０５），该组病变较糖尿病组轻。结论糖尿病可抑制激肽系统的活性，而补充胰激肽释放酶对糖尿病肾病的发展有一定的抑制作用。Objective To observe the effect of diabetes on the activation of kinin-system and the role of the system in development of diabetic nephropathy. Methods The TKA activation was measured and the function of kinin-system was changed by the antagonist of bradykinin B2 receptor-HOE 140 and kallikrein. Results The activation of TKA decreased sharply at 18 week in diabetic acts and was much lower than the levels of TKA at & week or in control rats (P<0. 001). The activation of TKA was higher in kallikrein-treated rats than in diabetic rats (P<0.05). The measuered parameters connected with diabetic nephropathy was much better than in the diabetic control (P<0. 05). Conclusion The activation of kinin-system was inhibited in diabetes. The improvement of the system's activation could be benefit to diabetic nephropathy.

关 键 词：糖尿病肾病 缓激肽受体阻滞剂 激肽 激肽释放酶 

分 类 号：R587.2[医药卫生—内分泌]