Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/42348
Title: Functional, biochemical, and molecular investigations of renal kallikrein-kinin system in diabetic rats
Authors: Tschope, C.
Reinecke, A.
Seidl, U.
Yu, M.
Gavriluk, V
Riester, U.
Gohlke, P.
Graf, K.
Bader, M.
Hilgenfeldt, U.
Pesquero, João Bosco [UNIFESP]
Ritz, E.
Unger, T.
Free Univ Berlin
Univ Kiel
Univ Heidelberg
Max Delbruck Ctr Mol Med
Humboldt Univ
Universidade Federal de São Paulo (UNIFESP)
Keywords: diabetic nephropathy
kininogen
neutral endopeptidase 24.11
angiotensin-converting enzyme
bradykinin B-2 receptor
streptozotocin
Issue Date: 1-Dec-1999
Publisher: Amer Physiological Soc
Citation: American Journal Of Physiology-heart And Circulatory Physiology. Bethesda: Amer Physiological Soc, v. 277, n. 6, p. H2333-H2340, 1999.
Abstract: A reduction of renal kallikrein has been found in non-insulin-treated diabetic individuals, suggesting that an impaired renal kallikreinkinin system (KKS) contributes to the development of diabetic nephropathy. We analyzed relevant components of the renal KKS in non-insulin-treated streptozotocin (STZ)-induced diabetic rats. Twelve weeks after a single injection of STZ, rats were normotensive and displayed hyperglycemia, polyuria, proteinuria, and reduced glomerular filtration rate. Blood bradykinin (BK) levels and prekallikrein activity were significantly increased compared with controls. Renal kallikrein activity was reduced by 70%, whereas urinary BK levels were increased up to threefold. Renal kininases were decreased as indicated by a 3-fold reduction in renal angiotensin-converting enzyme activity and a 1.8-fold reduction in renal expression of neutral endopeptidase 24.11. Renal cortical expression of kininogen and Bg receptors was enhanced to 1.4 and 1.8-fold, respectively Our data suggest that increased urinary BK levels found in severely hyperglycemic STZ-diabetic rats are related to increased filtration of components of the plasma KKS and/or renal kininogen synthesis in combination with decreased renal kinin-degrading activity. Thus, despite reduced renal kallikrein synthesis, renal KKS is activated in the advanced stage of diabetic nephropathy.
URI: http://repositorio.unifesp.br/11600/42348
ISSN: 0363-6135
Other Identifiers: http://ajpheart.physiology.org/content/277/6/H2333
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