Carretero O A, Scicli A G
Klin Wochenschr. 1978;56 Suppl 1:113-25. doi: 10.1007/BF01477462.
The kallikrein-kinin system in the kidney is localized in the distal nephron, where it appears to be linked to processes that control water and electrolyte excretion. Some evidence exists that the effect of the renal kallikrein-kinin system is partially mediated by the release of prostaglandins. It has not yet been determined whether endogenous kinins affect the function of the nephron directly or indirectly by changes in renal blood flow distribution. Further, a number of studies in animals and humans indicates that kallikrein excretion is decreased in most types of hypertension, with the exception of hypertension caused by an excess of mineralocorticoids (where kallikrein is increased). In rats susceptible to the hypertensive effect of salt, kallikrein is conspicuously decreased. In renal diseases, urinary kallikrein excretion is also decreased. Finally, it still needs to be determined whether or not low kallikrein excretion is a pathogenetic factor in hypertension and renal diseases.
肾脏中的激肽释放酶-激肽系统定位于远端肾单位，在那里它似乎与控制水和电解质排泄的过程相关。有证据表明，肾脏激肽释放酶-激肽系统的作用部分是由前列腺素的释放介导的。内源性激肽是直接影响肾单位功能，还是通过肾血流分布的变化间接影响肾单位功能，目前尚未确定。此外，多项针对动物和人类的研究表明，除了由盐皮质激素过多引起的高血压（这种情况下激肽释放酶增加）外，大多数类型的高血压患者激肽释放酶排泄量会降低。在对盐的高血压作用敏感的大鼠中，激肽释放酶明显减少。在肾脏疾病中，尿激肽释放酶排泄量也会降低。最后，低激肽释放酶排泄是否为高血压和肾脏疾病的致病因素仍有待确定。
