Renal Protective Role of Bradykinin B1 Receptor in Stroke-Prone Spontaneously Hypertensive Rats
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<B>The kallikrein-kinin system plays important roles in blood pressure regulation, metabolism of electrolytes and organ protection. Although the bradykinin B2 receptor (B2R) has been reported to be involved in most of these effects, a role of the bradykinin B1 receptor (B1R) has also been noted recently. The aim of this study was to determine the role of renal B1R in stroke-prone spontaneously hypertensive rats (SHR-SP). Sixteen-week-old SHR-SP and Wistar Kyoto rats (WKY) as a control were used in the experiments. A high level of B1R mRNA was detected in SHR-SP, while the expression in WKY was almost undetectable. Immunohistochemistry revealed a B1R protein in the renal tubules and glomeruli in SHR-SP. The acute injection of a B1R agonist into SHR-SP increased urinary NO<SUB><I>x</I></SUB> excretion to a level up to 5-fold higher than that in the SHR-SP treated with vehicle. The infusion of B1R antagonist for 4 weeks resulted in a significant elevation of blood pressure and urinary albumin excretion and a decrease in urinary NO<SUB><I>x</I></SUB> excretion in SHR-SP. The administration of B1R antagonist resulted in renal interstitial and glomerular fibrosis in SHR-SP. Moreover, the expressions of transforming growth factor (TGF) β1 protein and collagen III mRNA in SHR-SP treated with B1R antagonist were significantly higher than those of SHR-SP treated with a vehicle. The expression and phosphorylation of extracellular signal-regulated protein kinase (ERK) and p38, but not c-Jun N-terminal kinase (JNK), were significantly increased in the SHR-SP treated with B1R antagonist. These results indicated that renal B1R might be over-expressed in a high blood pressure condition, and that this up-regulated B1R may play an important role in renal protection by inhibiting renal fibrosis <I>via</I> an increase of NO production and a suppression of TGFβ1 expression and mitogen-activated protein kinase (ERK and p38) phosphorylation. (<I>Hypertens Res</I> 2004; 27: 399-408)</B>
- 日本高血圧学会の論文
日本高血圧学会 | 論文
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