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Title: Myocardial expression of rat bradykinin receptors and two tissue kallikrein genes in experimental diabetes
Authors: Tschope, C.
Walther, T.
Yu, M. H.
Reinecke, A.
Koch, M.
Seligmann, C.
Heringer, S. B.
Pesquero, J. B.
Bader, M.
Schultheiss, H. P.
Unger, T.
Free Univ Berlin
Max Delbruck Ctr Mol Med
Univ Kiel
Universidade Federal de São Paulo (UNIFESP)
Keywords: kallikrein
diabetic cardiopathy
B-1 receptor
B-2 receptor
Issue Date: 15-Oct-1999
Publisher: Elsevier B.V.
Citation: Immunopharmacology. Amsterdam: Elsevier B.V., v. 44, n. 1-2, p. 35-42, 1999.
Abstract: To characterize the role of the kallikrein-kinin system in diabetic cardiopathy, we studied the effect of streptozotocin (STZ) on the regulation of the myocardial bradykinin (BK) receptors, the B-1 and B-2 type, and two tissue kallikrein genes, rat kallikrein 1 (rKLK1) and rKLK7, in severely hyperglycemic rats. Experiments were performed in STZ-induced diabetic male Wistar rats (n = 7) and compared to controls (n = 7). After extraction of myocardial total RNA, specific oligonucleotides were used to generate reverse transcription PCR (RT-PCR) products from myocardial rKLK1 and rKLK7 mRNA. Southern blot analyses of these RT-PCR products were hybridized with appropriate gene-specific oligonucleotide probes. Myocardial B-1 and B-2 receptor expression were analyzed by RNase protection assays using specific probes from the coding region of the receptor genes. Twelve weeks after diabetes induction, the rats were normotensive and hyperglycemic and polyuric. We observed an impairment of the main myocardial kinin-forming enzymes, indicated by a reduction of the expression of both, rKLK1 and rKLK7. At this time the myocardial expression of the B-1 receptor was not detectable in either group. Thus, the B-1 receptor does not play a regulatory role in either the healthy or in STZ-diabetic heart. in contrast, the B-2-receptor expression was detectable but did not differ significantly in either group. the reduced synthesis of myocardial tissue KLK implies a reduced capacity to generate BK in diabetic rats. This reduction is not compensated by elevated BK receptor levels. We suggest that alterations of the KKS may contribute to myocardial dysfunction in diabetes mellitus. (C) 1999 Elsevier Science B.V. All rights reserved.
ISSN: 0162-3109
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