کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2554693 | 1124983 | 2006 | 7 صفحه PDF | دانلود رایگان |

AimTo investigate the relaxation effect and underlying mechanism of U50,488H (a selective κ-opioid receptor agonist) in pulmonary artery in the rat.MethodsIsolated pulmonary artery ring was perfused and the tension of the vessel was measured.ResultsU50,488H relaxed the pulmonary artery ring in a dose-dependent manner and the effect was abolished by nor-binaltorphimine, a selective κ-opioid receptor antagonist. The relaxation effect of U50,488H in pulmonary artery was partially endothelium-dependent and was significantly attenuated in the presence of L-NAME. The relaxation effect of U50,488H was significantly attenuated by KV channel blocker 4-AP (4-aminopyridine), but not by glibenclamide (ATP-sensitive K+ channel blocker) nor TEA (tetraethylamonium, Ca2+-activated K+ channel blocker). Further study also showed that endothelium denudation and 4-AP have an additive inhibitory effect on pulmonary artery relaxation caused by U50,488H.Conclusionκ-opioid receptor activation by U50,488H relaxes pulmonary artery via two separate pathways: one is endothelium-derived nitric oxide, the other is KV channel in pulmonary artery smooth muscle.
Journal: Life Sciences - Volume 78, Issue 21, 18 April 2006, Pages 2516–2522