Vio C P, Olavarría V, González C, Nazal L, Córdova M, Balestrini C
Departamento de Ciencias Fisiológicas, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile.
Biol Res. 1998;31(3):305-22.
The kallikrein kinin system is a tissue-derived system with potent renal and cardiovascular effects. Within the kidney, the components of the kallikrein kinin system (kallikrein, kininogen, kinins, kininases, kinin receptors and mediators/modulators) originate from or are located in discrete segments of the nephron in highly specialized cells which determine its physiological effects. The kallikrein system acts on the kidney in a paracrine fashion in two anatomical microenvironments where the system regulates glomerular function, renal hemodynamics, and salt and water excretion. Impairment of the renal kallikrein system contributes to the development of hypertension, in particular to the salt-sensitive hypertension, and other pathologies like diabetes. There are several links between the vasodepressor kallikrein system and the vasopressor renin system which are relevant to normal renal function and to the pathophysiology of hypertension and renal diseases. Local induction of kininase II or angiotensin converting enzyme in the kidney could be a novel mechanism contributing to the renal damage in hypertension and other renal diseases. This review evaluates cellular and functional aspects of the renal kallikrein system with emphasis placed on the cellular localization of its components along the nephron, the links to other vasoactive systems, and the contribution of the system to the pathogenesis of hypertension.
激肽释放酶 - 激肽系统是一个源自组织的系统，对肾脏和心血管系统具有强大作用。在肾脏内部，激肽释放酶 - 激肽系统的组成部分（激肽释放酶、激肽原、激肽、激肽酶、激肽受体以及介质/调节剂）源自肾单位的离散节段或位于其中高度特化的细胞内，这些细胞决定了该系统的生理效应。激肽释放酶系统以旁分泌方式在两个解剖学微环境中作用于肾脏，在这些微环境中该系统调节肾小球功能、肾血流动力学以及盐和水的排泄。肾脏激肽释放酶系统受损会导致高血压的发生，尤其是盐敏感性高血压，以及糖尿病等其他病症。血管舒张性激肽释放酶系统与血管收缩性肾素系统之间存在若干关联，这些关联与正常肾功能以及高血压和肾脏疾病的病理生理学相关。肾脏中激肽酶II或血管紧张素转换酶的局部诱导可能是导致高血压和其他肾脏疾病肾损伤的一种新机制。本综述评估了肾脏激肽释放酶系统的细胞和功能方面，重点关注其组成部分沿肾单位的细胞定位、与其他血管活性系统的联系以及该系统对高血压发病机制的贡献。
