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Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase
Despite the complex vascular effects of dexmedetomidine (DEX), its actions on human pulmonary resistance arteries remain unknown. The present study tested the hypothesis that DEX inhibits vascular tension in human pulmonary arteries through the endothelial nitric oxide synthase (eNOS) mediated produ...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Physiological Society and The Korean Society of Pharmacology
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5014990/ https://www.ncbi.nlm.nih.gov/pubmed/27610030 http://dx.doi.org/10.4196/kjpp.2016.20.5.441 |
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author | Nong, Lidan Ma, Jue Zhang, Guangyan Deng, Chunyu Mao, Songsong Li, Haifeng Cui, Jianxiu |
author_facet | Nong, Lidan Ma, Jue Zhang, Guangyan Deng, Chunyu Mao, Songsong Li, Haifeng Cui, Jianxiu |
author_sort | Nong, Lidan |
collection | PubMed |
description | Despite the complex vascular effects of dexmedetomidine (DEX), its actions on human pulmonary resistance arteries remain unknown. The present study tested the hypothesis that DEX inhibits vascular tension in human pulmonary arteries through the endothelial nitric oxide synthase (eNOS) mediated production of nitric oxide (NO). Pulmonary artery segments were obtained from 62 patients who underwent lung resection. The direct effects of DEX on human pulmonary artery tension and changes in vascular tension were determined by isometric force measurements recorded on a myograph. Arterial contractions caused by increasing concentrations of serotonin with DEX in the presence or absence of L-NAME (endothelial nitric oxide synthase inhibitor), yohimbine (α(2)-adrenoceptor antagonist) and indomethacin (cyclooxygenase inhibitor) as antagonists were also measured. DEX had no effect on endothelium-intact pulmonary arteries, whereas at concentrations of 10(–8)~10(–6) mol/L, it elicited contractions in endothelium-denuded pulmonary arteries. DEX (0.3, 1, or 3×10(–9) mmol/L) inhibited serotonin-induced contraction in arteries with intact endothelium in a dose-dependent manner. L-NAME and yohimbine abolished DEX-induced inhibition, whereas indomethacin had no effect. No inhibitory effect was observed in endothelium-denuded pulmonary arteries. DEX-induced inhibition of vasoconstriction in human pulmonary arteries is mediated by NO production induced by the activation of endothelial α(2)-adrenoceptor and nitric oxide synthase. |
format | Online Article Text |
id | pubmed-5014990 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | The Korean Physiological Society and The Korean Society of Pharmacology |
record_format | MEDLINE/PubMed |
spelling | pubmed-50149902016-09-08 Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase Nong, Lidan Ma, Jue Zhang, Guangyan Deng, Chunyu Mao, Songsong Li, Haifeng Cui, Jianxiu Korean J Physiol Pharmacol Original Article Despite the complex vascular effects of dexmedetomidine (DEX), its actions on human pulmonary resistance arteries remain unknown. The present study tested the hypothesis that DEX inhibits vascular tension in human pulmonary arteries through the endothelial nitric oxide synthase (eNOS) mediated production of nitric oxide (NO). Pulmonary artery segments were obtained from 62 patients who underwent lung resection. The direct effects of DEX on human pulmonary artery tension and changes in vascular tension were determined by isometric force measurements recorded on a myograph. Arterial contractions caused by increasing concentrations of serotonin with DEX in the presence or absence of L-NAME (endothelial nitric oxide synthase inhibitor), yohimbine (α(2)-adrenoceptor antagonist) and indomethacin (cyclooxygenase inhibitor) as antagonists were also measured. DEX had no effect on endothelium-intact pulmonary arteries, whereas at concentrations of 10(–8)~10(–6) mol/L, it elicited contractions in endothelium-denuded pulmonary arteries. DEX (0.3, 1, or 3×10(–9) mmol/L) inhibited serotonin-induced contraction in arteries with intact endothelium in a dose-dependent manner. L-NAME and yohimbine abolished DEX-induced inhibition, whereas indomethacin had no effect. No inhibitory effect was observed in endothelium-denuded pulmonary arteries. DEX-induced inhibition of vasoconstriction in human pulmonary arteries is mediated by NO production induced by the activation of endothelial α(2)-adrenoceptor and nitric oxide synthase. The Korean Physiological Society and The Korean Society of Pharmacology 2016-09 2016-08-26 /pmc/articles/PMC5014990/ /pubmed/27610030 http://dx.doi.org/10.4196/kjpp.2016.20.5.441 Text en Copyright © Korean J Physiol Pharmacol http://creativecommons.org/licenses/by-nc/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Nong, Lidan Ma, Jue Zhang, Guangyan Deng, Chunyu Mao, Songsong Li, Haifeng Cui, Jianxiu Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase |
title | Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase |
title_full | Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase |
title_fullStr | Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase |
title_full_unstemmed | Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase |
title_short | Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase |
title_sort | dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5014990/ https://www.ncbi.nlm.nih.gov/pubmed/27610030 http://dx.doi.org/10.4196/kjpp.2016.20.5.441 |
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