What have we learned about the kallikrein-kinin and renin-angiotensin systems in neurological disorders?

Figure 4 Schematic representation of the role of angiotensin converting enzyme in the renin-angiotensin and kallikrein-kinin systems. A: Conversion of AngI into AngII by angiotensin converting enzyme (ACE); B: Bradykinin (BK) degradation by ACE. Physiological effects on the renin-angiotensin system mediated by Ang II type 1 receptor (AT1R) include: vasoconstriction, neuroinflammation, and increased sympathetic nerve activity. Those mediated by Ang II type 2 receptor (AT2R) include cell differentiation and vasodilation. The effects on the kallikrein-kinin system, mediated by kinins, bradykinin and their receptor (B2R) also include vasodilation and hypotension, via the release of nitric oxide (NO), prostacyclins and endothelium-derived hyperpolarizing factor (EDHF). It is important to emphasize that in human pathological conditions, the use of ACE inhibitors results in downregulation of AngII production. In this sense, the kallikrein-kinin system is upregulated and the physiological effects of kinins are potentiated, as all kinin-related peptides are less hydrolyzed by ACE inhibition.