Guder W G, Hallbach J
Institut für Klinische Chemie, Städtisches Krankenhaus München-Bogenhausen.
Klin Wochenschr. 1988 Sep 15;66(18):849-56. doi: 10.1007/BF01728946.
The complete renal kallikrein kinin system has recently been localized in defined nephron segments. Kallikrein was found to be formed and secreted by connecting tubule cells in the late distal convoluted tubule, whereas kininogen and a novel kininase were located in collecting tubules. Kinins were shown to act on collecting tubule as well as medullary interstitial cells and the renal vasculature. The literature on interactions of this system with renal sodium transport is conflicting. Renal and urinary kallikrein was found to be increased under sodium restricted conditions, whereas kinin has a diuretic and natriuretic effect in the collecting tubule, when added from the basolateral surface. On the other hand renal kallikrein activity and connecting tubule cell morphology change in parallel with dietary potassium load indicating a coupling to potassium secretion. The possible role of the renal kallikrein kinin system in regulating collecting tubule function by tubular and vascular effects is outlined in spite of many open questions which remain to be answered.
完整的肾激肽释放酶 - 激肽系统最近已定位在特定的肾单位节段中。发现激肽释放酶由远曲小管末端的连接小管细胞形成并分泌，而激肽原和一种新型激肽酶位于集合小管中。已表明激肽作用于集合小管以及髓质间质细胞和肾血管系统。关于该系统与肾钠转运相互作用的文献存在矛盾之处。在钠限制条件下，肾和尿中的激肽释放酶增加，而当从基底外侧表面添加时，激肽在集合小管中具有利尿和利钠作用。另一方面，肾激肽释放酶活性和连接小管细胞形态随饮食钾负荷平行变化，表明与钾分泌相关。尽管仍有许多未解决的问题，但本文概述了肾激肽释放酶 - 激肽系统通过肾小管和血管效应调节集合小管功能的可能作用。
