Bradykinin release and inactivation in brain of rats submitted to an experimental model of Alzheimer's disease.
The kallikrein-kinin system is involved in a variety of physiological and pathological processes. Components of this system, identified in rat and human brains, can be altered in neurodegenerative processes such as Alzheimer's disease. Here, we studied kinin release and its inactivation in rats submitted to chronic cerebroventricular infusion of beta-amyloid (Abeta) peptide. Neurodegeneration was confirmed by histological analysis of brain samples. In cerebrospinal fluid of animals infused with Abeta, bradykinin concentration was increased, as determined by radioimmunoassay. However, in the brain of Abeta group, we only detected the tripeptide Arg-Pro-Pro, purified by reversed-phase chromatography and characterized by liquid chromatography-electrospray ionization mass spectrometry. This fragment of bradykinin indicated the possible participation of kinin-processing enzymes in the brain such as a prolyl oligopeptidase.
Iores-Marçal
Lígia M
LM
Department of Biochemistry, Escola Paulista de Medicina, Universidade Federal de Sao Paulo, Rua Três de Maio 100, 04044-020, S. Paulo, SP, Brazil. iores.bioq@epm.br
Viel
Tânia A
TA
Buck
Hudson Sousa
HS
Nunes
Viviane A
VA
Gozzo
Andrezza J
AJ
Cruz-Silva
Ilana
I
Miranda
Antonio
A
Shimamoto
Kazuaki
K
Ura
Nobuyuki
N
Araujo
Mariana S
MS
D000544:Alzheimer Disease / Q000378:metabolism*; D000818:Animals; D001920:Bradykinin / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D001921:Brain / Q000378:metabolism*; D004195:Disease Models, Animal; D051381:Rats
D001920:Bradykinin