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- W2111886628 abstract "The bradykinin B 1 receptor (B 1 R) is normally absent under physiological conditions, but is highly inducible during inflammatory conditions or following tissue damage. The present study attempted to determine some of the mechanisms underlying B 1 R upregulation following tissue injury in rat portal vein. Damage induced by tissue isolation and in vitro incubation caused a significant and time-dependent increase in des-Arg 9 –bradykinin (des-Arg 9 –BK) responsiveness that paralleled the B 1 R mRNA expression, as confirmed by real-time quantitative PCR. In vitro incubation of rat portal vein also induced the activation of some members of the mitogen activated protein kinase (MAPK) family, namely, extracellular signal-regulated kinase (ERK), c-Jun NH 2 -terminal kinase (JNK), and p38 MAPK, an effect accompanied by degradation of the inhibitory protein IκBα and translocation of nuclear transcription factor-κB (NF-κB) to the nucleus. The blockade of p38 MAPK, JNK or NF-κB, but not ERK pathways with selective inhibitors, resulted in a significant reduction of the upregulated contractile response caused by the selective B 1 R agonist des-Arg 9 –BK, and largely prevented the induction of B 1 R mRNA expression in the rat portal vein. Together, these results demonstrate that in vitro tissue damage induces activation of several intracellular signaling pathways that have a key role in the control of B 1 R expression. B 1 R could exert a pivotal role in the development of the cardiovascular response associated with vascular damage." @default.
- W2111886628 created "2016-06-24" @default.
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- W2111886628 date "2004-05-28" @default.
- W2111886628 modified "2023-10-17" @default.
- W2111886628 title "Bradykinin B<sub>1</sub>Receptor Expression Induced by Tissue Damage in the Rat Portal Vein" @default.
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- W2111886628 doi "https://doi.org/10.1161/01.res.0000128404.65887.08" @default.
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