The renal kallikrein-kinin system in human and in experimental hypertension

Abstract

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.