ArticleBritish journal of pharmacology2001
Nitric oxide-mediated modulation of the endothelin-1 signalling pathway in the human cardiovascular system.
Article in British journal of pharmacology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 66 citations in OpenAlex.
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- Pulmonary Hypertension in Acute and Chronic High Altitude Maladaptation Disorders.International journal of environmental research and public health · 2021Review
- Pharmacological regulation of outflow resistance distal to Schlemm's canal.American journal of physiology. Cell physiology · 2018Article
- Endothelin.Pharmacological reviews · 2016Review
- Conceptual approaches for treatment of phosgene inhalation-induced lung injury.Toxicology letters · 2016Article
- The effect of ozone on blood pressure in DOCA-salt-induced hypertensive rats.International journal of clinical and experimental medicine · 2015Article
- Immunosuppressive/anti-inflammatory cytokines directly and indirectly inhibit endothelial dysfunction--a novel mechanism for maintaining vascular function.Journal of hematology & oncology · 2014Review
- Exercise limits the production of endothelin in the coronary vasculature.American journal of physiology. Heart and circulatory physiology · 2011Article
- Alterations in endothelial control of the pulmonary circulation in exercising swine with secondary pulmonary hypertension after myocardial infarction.The Journal of physiology · 2007Article
- Nitric oxide modulates renal vasoconstrictor effect of endothelin-1 in conscious lambs.Pediatric nephrology (Berlin, Germany) · 2005Article
- Nitric oxide blunts the endothelin-mediated pulmonary vasoconstriction in exercising swine.The Journal of physiology · 2005Article
- CRF2 receptors are highly expressed in the human cardiovascular system and their cognate ligands urocortins 2 and 3 are potent vasodilators.British journal of pharmacology · 2004Article
- Comparison of vasodilators in human internal mammary artery: ghrelin is a potent physiological antagonist of endothelin-1.British journal of pharmacology · 2002Article
- Physiological antagonism of endothelin-1 in human conductance and resistance coronary artery.British journal of pharmacology · 2001Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We studied the ability of nitric oxide (NO) to physiologically antagonize endothelin-1 (ET-1) induced constrictions in human internal mammary artery (IMA). We also investigated the hypothesis that NO interacts directly with ET-receptor binding in human heart and aorta. 2. ET-1 potently contracted IMA (EC(50) 6.86 nM, 95% CI: 3.5 - 13.4 nM; n=12). The constrictor response to 10 nM ET-1 was fully reversed by the NO-donor diethylamine NONOate (DEA/NO; EC(50) 2.0 microM, 95% CI: 0.8 - 4.8 microM; n=5). The guanylate cyclase inhibitor ODQ (100 microM) reduced the response to DEA/NO but did not abolish it (E(MAX) 50.9+/-8.5% in the presence of ODQ; 113.0+/-8.4%, control). 3. The increase in cyclic GMP by 30 microM DEA/NO was abolished in the presence of 100 microM ODQ (n=6). 4. In saturation binding experiments the NO-donor Diethyltriamine NONOate (DETA/NO; 1 mM) caused a 90% reduction in maximum binding of [(125)I]-ET-1 in human heart, without affecting the affinity. This reduction in binding was abolished by haemoglobin. Pre-incubating either the radiolabel or the tissue with NO-donors did not reduce binding. A similar effect was observed in aortic smooth muscle. 5. We have shown that DEA/NO is able to reverse ET-1-induced contractions in the human vasculature. The binding studies suggest a direct interaction between NO and the ET receptor or receptor-ligand complex in human ventricular and aortic tissue. NO is released continuously in vivo, thus this apparent modification of ET-receptor binding may provide an additional mechanism by which NO counter-balances the effects of ET.
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