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Korean J Anesthesiol. 1995 Jun;28(6):739-746. Korean. Original Article.
Kim WO , Kil HK , Kwak YR , Lee KW .
Department of Anesthesiology, Yonsei University College of Medicine, Seoul, Korea.
Abstract

The mechanism of vasodilation induced by fentanyl was investigated using isolated rat thoracic aortic rings. Rings were contracted with norepinephrine(10(-7) M, NE) and potassium chloride(40 mM, KC1) with and without endothelium Fentanyl (10(-9)-10(-5) M) produced dose-dependent relaxation and had no significant effect from endothelium(intact and denuded rings, test with 3X10(-4) M LNAME, N-nitro-L-arginine methyl ester). Pretreatment of indomethacin(2.5X10(-3) M, inhibitor of cyclooxygenase) failed to influence of cumulative dose-response curves. RD(50)(50% relaxation dose) and KC1/NE ratio as potency difference of fentanyl, verapamil(10(-8)-10(-5) M, Ca2+ channel blocker), nitroglycerin(10(-10)-10(-5) M, activator of guanylate cyclase) were not similar. Fentanyl and control(distilled water) were not demonstrated any different contraction produced by incremental addition of Ca2+ to aortic rings exposed to Ca2+ free, K+ -depolarized(100 mM KCl) solution(extracellular Ca2+ influx). But fentanyl had effect on intracellular Ca2+ release elicited by caffeine(20 mM) and NE(10(-7) M) indicated by dose-dependent inhibition of contraction in Ca2+ free solution. We conclude that, in rat aorta, fentanyl-induced relaxation is endothelium-independent but mediated by inhibition of alpha-adrenoceptors operated intracellular Ca2+ release (inhibition of contraction by NE) and caffeine-induced Ca2+ release from store.

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