RESUMO
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.