作者: Jean-Pierre Girolami , Nelly Blaes , Nadine Bouby , François Alhenc-Gelas
DOI: 10.1007/978-3-319-06683-7_6
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摘要: Genetic manipulation of the kallikrein-kinin system (KKS) in mice, with either gain or loss function, and study human genetic variability KKS components which has been well documented at phenotypic genomic level, have allowed recognizing physiological role health disease. This especially cardiovascular kidney. Kinins are produced slow rate most organs resting condition and/or inactivated quickly. Yet is involved arterial function renal tubular function. In several pathological situations, kinin production increases, receptor synthesis upregulated, kinins play an important role, whether beneficial detrimental, disease outcome. setting ischemic, diabetic hemodynamic aggression, release by tissue kallikrein protects against organ damage, through B2 B1 bradykinin activation, depending on for ischemic heart, kidney skeletal muscle, where activity reduces oxidative stress, limits necrosis fibrosis promotes angiogenesis. On other hand, some situations plasma prekallikrein inappropriately activated, excess local systemic circulation oedema hypotension. Putative therapeutic application these clinical experimental findings current pharmacological development discussed chapter.