Published online May 26, 2014. doi: 10.4331/wjbc.v5.i2.130
Revised: February 10, 2014
Accepted: March 17, 2014
Published online: May 26, 2014
The kallikrein-kinin system (KKS) is an intricate endogenous pathway involved in several physiological and pathological cascades in the brain. Due to the pathological effects of kinins in blood vessels and tissues, their formation and degradation are tightly controlled. Their components have been related to several central nervous system diseases such as stroke, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, epilepsy and others. Bradykinin and its receptors (B1R and B2R) may have a role in the pathophysiology of certain central nervous system diseases. It has been suggested that kinin B1R is up-regulated in pathological conditions and has a neurodegenerative pattern, while kinin B2R is constitutive and can act as a neuroprotective factor in many neurological conditions. The renin angiotensin system (RAS) is an important blood pressure regulator and controls both sodium and water intake. AngII is a potent vasoconstrictor molecule and angiotensin converting enzyme is the major enzyme responsible for its release. AngII acts mainly on the AT1 receptor, with involvement in several systemic and neurological disorders. Brain RAS has been associated with physiological pathways, but is also associated with brain disorders. This review describes topics relating to the involvement of both systems in several forms of brain dysfunction and indicates components of the KKS and RAS that have been used as targets in several pharmacological approaches.
Core tip: This review is a description of the involvement of the kallikrein-kinin and renin-angiotensin systems in neurological disorders. We describe all components of both systems, relating them to several brain diseases such as Alzheimer’s disease, Parkinson’s disease, epilepsy, multiple sclerosis, blood brain barrier disruption, stroke and inflammation, including the involvement of each molecule, their receptor and specific enzymes in individual pathologies. We also show that brain homeostasis depends on a dynamic balance between the kallikrein-kinin and renin-angiotensin systems.