Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase
| Autor: | Jue Ma, Lidan Nong, Chunyu Deng, Jianxiu Cui, Songsong Mao, Haifeng Li, Guangyan Zhang |
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| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
Serotonin
Physiology 030204 cardiovascular system & hematology Pharmacology Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine 030202 anesthesiology Enos medicine.artery polycyclic compounds Medicine Human pulmonary arteries biology business.industry biology.organism_classification Yohimbine Nitric oxide synthase chemistry Vasoconstriction Anesthesia Pulmonary artery biology.protein Original Article Cyclooxygenase medicine.symptom business hormones hormone substitutes and hormone antagonists Dexmedetomidine Myograph medicine.drug |
| Zdroj: | The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology |
| ISSN: | 1226-4512 |
| Popis: | 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 (α2-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 α2-adrenoceptor and nitric oxide synthase. |
| Databáze: | OpenAIRE |
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