Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase.
10.4196/kjpp.2016.20.5.441
- Author:
Lidan NONG
1
;
Jue MA
;
Guangyan ZHANG
;
Chunyu DENG
;
Songsong MAO
;
Haifeng LI
;
Jianxiu CUI
Author Information
1. Department of Anesthesiology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. cuijianxiu@163.com
- Publication Type:Original Article
- Keywords:
Dexmedetomidine;
Human pulmonary arteries;
Nitric oxide;
Serotonin;
Vasoconstriction
- MeSH:
Arteries;
Dexmedetomidine*;
Endothelium;
Humans;
Indomethacin;
Lung;
NG-Nitroarginine Methyl Ester;
Nitric Oxide;
Nitric Oxide Synthase;
Nitric Oxide Synthase Type III*;
Pulmonary Artery;
Serotonin;
Vasoconstriction*;
Yohimbine
- From:The Korean Journal of Physiology and Pharmacology
2016;20(5):441-447
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
