Relaxing Responses to Hydrogen Peroxide and Nitric Oxide in Human Pericardial Resistance Arteries Stimulated with Endothelin‐1
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| Název: | Relaxing Responses to Hydrogen Peroxide and Nitric Oxide in Human Pericardial Resistance Arteries Stimulated with Endothelin‐1 |
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| Autoři: | Lars Riber, Maria Bloksgaard, Thomas Leurgans, Akhmadjon Irmukhamedov, Jo G. R. De Mey |
| Zdroj: | Leurgans, T M, Bloksgaard, M, Irmukhamedov, A, Riber, L P & De Mey, J G R 2018, ' Relaxing Responses to Hydrogen Peroxide and Nitric Oxide in Human Pericardial Resistance Arteries Stimulated with Endothelin-1 ', Basic & Clinical Pharmacology & Toxicology, vol. 122, no. 1, pp. 74–81 . https://doi.org/10.1111/bcpt.12843 |
| Informace o vydavateli: | Wiley, 2017. |
| Rok vydání: | 2017 |
| Témata: | Male, Nitroprusside, 0301 basic medicine, Endothelium, Vascular/drug effects, Vasodilator Agents, Nitric Oxide, Muscle, Smooth, Vascular, MECHANISMS, ACTIVATION, 03 medical and health sciences, 0302 clinical medicine, Pericardium/physiopathology, Humans, Nitric Oxide/pharmacology, Endothelium, Vasodilator Agents/pharmacology, Vascular/drug effects, Aged, HYPERPOLARIZING FACTOR, Cardiovascular Diseases/physiopathology, THERAPEUTIC TARGET, Endothelin-1, Coronary Vessels/drug effects, Vasodilation/drug effects, Endothelin-1/metabolism, Hydrogen Peroxide, Nitroprusside/pharmacology, CONCISE GUIDE, Coronary Vessels, DYSFUNCTION, 3. Good health, Vasodilation, CARDIOVASCULAR-DISEASE, RELAXATIONS, Cardiovascular Diseases, Muscle, Female, Smooth, Endothelium, Vascular, Muscle, Smooth, Vascular/drug effects, VASOCONSTRICTION, Pericardium, SYSTEM, Hydrogen Peroxide/pharmacology |
| Popis: | In human pericardial resistance arteries, effects of the endothelium‐dependent vasodilator bradykinin are mediated by NO during contraction induced by K+ or the TxA2 analogue U46619 and by H2O2 during contraction by endothelin‐1 (ET‐1), respectively. We tested the hypotheses that ET‐1 reduces relaxing effects of NO and increases those of H2O2 in resistance artery smooth muscle of patients with cardiovascular disease. Arterial segments, dissected from the parietal pericardium of 39 cardiothoracic surgery patients, were studied by myography during amplitude‐matched contractions induced by K+, the TXA2 analogue U46619 or ET‐1. Effects of the NO donor Na‐nitroprusside (SNP) and of exogenous H2O2 were recorded in the absence and presence of inhibitors of cyclooxygenases, NO synthases and small and intermediate conductance calcium‐activated K+ channels. During contractions induced by either of the three stimuli, the potency of SNP did not differ and was not modified by the inhibitors. In vessels contracted with ET‐1, the potency of H2O2 was on average and in terms of interindividual variability considerably larger than in K+‐contracted vessels. Both differences were not statistically significant in the presence of inhibitors of mechanisms of endothelium‐dependent vasodilatation. In resistance arteries from patients with cardiovascular disease, ET‐1 does not selectively modify smooth muscle relaxing responses to NO or H2O2. Furthermore, the candidate endothelium‐derived relaxing factor H2O2 also acts as an endothelium‐dependent vasodilator. |
| Druh dokumentu: | Article |
| Jazyk: | English |
| ISSN: | 1742-7843 1742-7835 |
| DOI: | 10.1111/bcpt.12843 |
| Přístupová URL adresa: | https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/bcpt.12843 https://pubmed.ncbi.nlm.nih.gov/28686356 https://cris.maastrichtuniversity.nl/en/publications/2de63969-65b9-41be-abea-2e4fd75d5488 https://doi.org/10.1111/bcpt.12843 https://onlinelibrary.wiley.com/doi/abs/10.1111/bcpt.12843 https://cris.maastrichtuniversity.nl/portal/en/publications/relaxing-responses-to-hydrogen-peroxide-and-nitric-oxide-in-human-pericardial-resistance-arteries-stimulated-with-endothelin1(2de63969-65b9-41be-abea-2e4fd75d5488).html https://www.ncbi.nlm.nih.gov/pubmed/28686356 https://europepmc.org/abstract/MED/28686356 https://cris.maastrichtuniversity.nl/en/publications/relaxing-responses-to-hydrogen-peroxide-and-nitric-oxide-in-human https://pubmed.ncbi.nlm.nih.gov/28686356/ https://portal.findresearcher.sdu.dk/da/publications/cb9ff3df-b8d7-43ca-8b7a-5fc473b8db13 https://doi.org/10.1111/bcpt.12843 https://portal.findresearcher.sdu.dk/da/publications/cb9ff3df-b8d7-43ca-8b7a-5fc473b8db13 |
| Rights: | Wiley Online Library User Agreement |
| Přístupové číslo: | edsair.doi.dedup.....73ba5906a985afe2601c210ea010bf8d |
| Databáze: | OpenAIRE |
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Nájsť tento článok vo Web of Science | Abstrakt: | In human pericardial resistance arteries, effects of the endothelium‐dependent vasodilator bradykinin are mediated by NO during contraction induced by K+ or the TxA2 analogue U46619 and by H2O2 during contraction by endothelin‐1 (ET‐1), respectively. We tested the hypotheses that ET‐1 reduces relaxing effects of NO and increases those of H2O2 in resistance artery smooth muscle of patients with cardiovascular disease. Arterial segments, dissected from the parietal pericardium of 39 cardiothoracic surgery patients, were studied by myography during amplitude‐matched contractions induced by K+, the TXA2 analogue U46619 or ET‐1. Effects of the NO donor Na‐nitroprusside (SNP) and of exogenous H2O2 were recorded in the absence and presence of inhibitors of cyclooxygenases, NO synthases and small and intermediate conductance calcium‐activated K+ channels. During contractions induced by either of the three stimuli, the potency of SNP did not differ and was not modified by the inhibitors. In vessels contracted with ET‐1, the potency of H2O2 was on average and in terms of interindividual variability considerably larger than in K+‐contracted vessels. Both differences were not statistically significant in the presence of inhibitors of mechanisms of endothelium‐dependent vasodilatation. In resistance arteries from patients with cardiovascular disease, ET‐1 does not selectively modify smooth muscle relaxing responses to NO or H2O2. Furthermore, the candidate endothelium‐derived relaxing factor H2O2 also acts as an endothelium‐dependent vasodilator. |
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| ISSN: | 17427843 17427835 |
| DOI: | 10.1111/bcpt.12843 |