ArticleBritish journal of pharmacology2004
The contractile action of leukotriene B4 in the guinea-pig lung involves a vascular component.
Article in British journal of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 32 citations in OpenAlex.
- Systemic Sclerosis: Elevated Levels of Leukotrienes in Saliva and Plasma Are Associated with Vascular Manifestations and Nailfold Capillaroscopic Abnormalities.International journal of environmental research and public health · 2021Article
- Review
- The acute phase of Trypanosoma cruzi infection is attenuated in 5-lipoxygenase-deficient mice.Mediators of inflammation · 2014Article
- Leukotrienes as modifiers of preclinical atherosclerosis?TheScientificWorldJournal · 2012Review
- Inflammatory signaling through leukotriene receptors in atherosclerosis.Current atherosclerosis reports · 2008Review
- Leukotriene B4 signaling through NF-kappaB-dependent BLT1 receptors on vascular smooth muscle cells in atherosclerosis and intimal hyperplasia.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
Leukotriene B4 (LTB4) is a potent leukocyte chemoattractant, acting on specific receptors, BLT receptors. The aim of this study was to examine the mechanism of action of LTB4 in the guinea-pig lung, using strips of lung parenchyma (GPLP), spirals of trachea (GPT) and bronchus (GPB) and rings of pulmonary artery (GPPA). Mechanical responses were studied in organ baths, and mediator release was assessed using enzyme immuno assay. LTB4 induced similar contractions of GPLP and GPPA, whereas LTB4 had only small contractile effects in GPT and GPB. In addition, the contractile response to LTB4 was reproduced in the human pulmonary artery. In the GPLP, the unselective BLT receptor antagonist ONO-4057 abolished the contractions induced by LTB4, whereas the selective BLT1 receptor antagonist U-75302 only partly inhibited the LTB4-induced contractions. In the GPPA, both antagonists abolished the response to LTB4. The effect of LTB4 in GPPA and GPLP was indirect and mediated by the release of thromboxane A2 and histamine, as supported by selective pharmacologic interventions and measurements of thromboxane B2 and histamine in the organ baths. In conclusion, the results indicate a new biological function of LTB4, namely to constrict isolated pulmonary arteries. Moreover, the findings suggest that the LTB4-induced contractions of GPPA were mediated by a BLT1 receptor, whereas BLT2 receptor activation accounted for a major part of the contraction of GPLP, making the latter preparation a suitable assay for BLT2 receptors. British Journal of Pharmacology (2004) 141, 449-456. doi:10.1038/sj.bjp.0705641
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