ArticleBritish journal of pharmacology1999
Inducible expression of the kinin B1 receptor in the endotoxemic heart: mechanisms of des-Arg9bradykinin-induced coronary vasodilation.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 70 citations in OpenAlex.
- Role of Endothelial Kinin B1 Receptor on the Membrane Potential of Transgenic Rat Aorta.Physiological research · 2022Article
- Comorbidities and inflammation associated with ovarian cancer and its influence on SARS-CoV-2 infection.Journal of ovarian research · 2021Review
- COVID-19 cytokine storm: The anger of inflammation.Cytokine · 2020Review
- Host kinin B1 receptor plays a protective role against melanoma progression.Scientific reports · 2016Article
- Article
- Exacerbation of DSS-induced colitis in mice lacking kinin B(1) receptors through compensatory up-regulation of kinin B(2) receptors: the role of tight junctions and intestinal homeostasis.British journal of pharmacology · 2013Article
- Article
- Differential regulation of inducible and endothelial nitric oxide synthase by kinin B1 and B2 receptors.Neuropeptides · 2010Review
- Predisposition to atherosclerosis and aortic aneurysms in mice deficient in kinin B1 receptor and apolipoprotein E.Journal of molecular medicine (Berlin, Germany) · 2009Article
- Increased susceptibility to endotoxic shock in transgenic rats with endothelial overexpression of kinin B(1) receptors.Journal of molecular medicine (Berlin, Germany) · 2008Article
- Kinin B1 receptors: key G-protein-coupled receptors and their role in inflammatory and painful processes.British journal of pharmacology · 2004Review
- Reduction of nitrite to nitric oxide during ischemia protects against myocardial ischemia-reperfusion damage.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Plasma extravasation mediated by lipopolysaccharide-induction of kinin B1 receptors in rat tissues.Mediators of inflammation · 2001Article
- Endotoxin sensitization to kinin B(1) receptor agonist in a non-human primate model: haemodynamic and pro-inflammatory effects.British journal of pharmacology · 2001Article
- Non-competitive pharmacological antagonism at the rabbit B(1) receptor.British journal of pharmacology · 2000Article
- Association between kinin B(1) receptor expression and leukocyte trafficking across mouse mesenteric postcapillary venules.The Journal of experimental medicine · 2000Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1 We have investigated the role of kinin B1 receptor induction in the endotoxemic rat heart and elucidated the mechanisms underlying B1 receptor-mediated coronary vasodilation. We also investigated the role of these receptors in endotoxin-induced hypotension. 2 Endotoxin treatment induced cardiac B1 receptor mRNA expression and promoted a coronary vasodilation response to des-Arg9bradykinin (DABK; ED50 = 149.4 pmol, n = 9) ex vivo peaking at 6 h. The B1 receptor antagonist des-Arg9-[Leu8]-BK (DALBK, 30 nM) significantly (P<0.05) inhibited the DABK-induced response (pA2 = 8.4, n = 5) whilst HOE140 (B2 receptor antagonist, 10 nM) was inactive (n = 4). 3 Removal of the endothelium or infusion with indomethacin (5 microM), but not L-NAME (300 microM) or ODQ (1 microM), inhibited (>85%, P<0.05, n = 5) the DABK-induced response. DABK caused a dose-dependent release of the prostacyclin metabolite, 6-keto-PGF1a (Emax = 0.3 ng ml-1, n = 6). 4 In vitro perfusion of hearts with endotoxin (1 microg ml-1, n = 6) or interleukin-1beta (5 ng ml-1, n = 6) induced B1 receptor mRNA expression and promoted a time-dependent vasodilation response to DABK. 5 Endotoxin treatment (6 h) in vivo promoted a hypotensive response to DABK (ED50 = 29.7 nmol kg-1, n = 10) which was antagonised by DALBK (3-6 nmol kg-1 min-1, P<0.05, n = 7). DALBK (3 nmol kg-1 min-1) and des-Arg10HOE140 (B1 receptor antagonist, 30 nmol kg-1 min-1) produced a 5.3% (n = 6, P<0.05) and 8.8% (n = 5, P<0.05) reversal, respectively, of endotoxin-induced hypotension. 6 In summary, we have shown that in endotoxemia activation of B1 receptors causes coronary vasodilation via endothelial prostacyclin release. Additionally, B1 receptor antagonists partially reversed endotoxin-induced hypotension. Therefore activation of B1 receptors may have a role to play in the vascular changes associated with endotoxemia.
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