ArticleThe Journal of physiology2001
Endothelial kinin B(1)-receptors are induced by myocardial ischaemia-reperfusion in the rabbit.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Different expression of connexin 43 between culprit arteries and non-culprit arteries and role of angiotensin II on expression of connexin 43 in non-culprit arteries.International journal of clinical and experimental pathology · 2018Article
- Predisposition to atherosclerosis and aortic aneurysms in mice deficient in kinin B1 receptor and apolipoprotein E.Journal of molecular medicine (Berlin, Germany) · 2009Article
- Kinin B1 receptors: key G-protein-coupled receptors and their role in inflammatory and painful processes.British journal of pharmacology · 2004Review
- Role of the bradykinin B2 receptor for the local and systemic inflammatory response that follows severe reperfusion injury.British journal of pharmacology · 2003Article
- Absence of ligand-induced regulation of kinin receptor expression in the rabbit.British journal of pharmacology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kinin B1-receptors are induced by various inflammatory stimuli. Since myocardial ischaemia-reperfusion results in inflammation, we questioned whether it could induce B1-receptor-dependent responses to des-Arg9-bradykinin (DBK). Thirty-six rabbits were submitted either to a 30 min coronary occlusion followed by a 3 h reperfusion or to a sham operation. The response to DBK was then tested in vivo on mean arterial pressure (MAP) and in vitro on isolated hearts and arterial rings. DBK induced a dose-dependent decrease in MAP in the ischaemia-reperfusion group (DBK, 10 microg kg(-1), intra-arterial: -12 +/- 2 vs. -5 +/- 2 mm Hg in the sham group, P < 0.02), which was significantly antagonised by [Leu8]-des-Arg9-bradykinin (LBK), a B1-receptor antagonist. Following ischaemia-reperfusion, isolated hearts responded to DBK by a decrease in coronary perfusion pressure greater than that of the sham group. DBK dose-dependently decreased the isometric force of isolated carotid rings (DBK, 10(-5) M: -9 +/- 2 vs. -1 +/- 2% in the sham group, P < 0.02) and mesenteric arteries (DBK, 10-6 M: -38 +/- 7% vs. -3 +/- 2 % in the sham group, P < 0.001). The vascular effects of DBK seen after ischaemia-reperfusion were significantly antagonised by LBK. The presence of B1-receptors in ischaemia-reperfusion animals was confirmed by immunolocalisation and Western blot analysis. This study demonstrates that myocardial ischaemia-reperfusion induces a global induction of functional kinin B1-receptors in the endothelium.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.