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논문 상세정보

흰쥐 대동맥에서 fluoxetine의 혈관 이완 효과

Vasorelaxant effect of fluoxetine in isolated rat aorta

Abstract

The vasorelaxant effect of serotonin reuptake inhibitor fluoxetine was investigated in rat isolated thoracic aorta. Fluoxetine induced a concentration-dependent relaxation in aorta precontracted with phenylephrine (PE) and KCl. These relaxations were suppressed by removal of the endothelium (-E) or pretreatment of nitric oxide synthase inhibitors, N(G)-nitro-L-arginine (L-NNA) and N(omega)-nitro-Larginine methyl ester (L-NAME), guanylate cyclase inhibitors, methylene blue (MB) and 1H-[1,2,4]oxadiazolo [4,3-a]quinoxalin-1-one (ODQ), and $Ca^{2+}$ channel blockers, nifedipine and verapamil, in PE-precontracted +E rings. However, fluoxetine-induced relaxations were not suppressed by pretreatment of $K^{+}$ channel blockers, tetrabutylammonium and glibenclamide, in PE-precontracted endothelium intact (+E) rings. The fluoxetine-induced relaxations were not suppressed by removal of the endothelium or pretreatment of LNNA and MB in KCl-precontracted +E rings. Also, fluoxetine inhibited PE-induced sustained contraction in +E rings. These inhibitory effects of fluoxetine on contractions could be reversed by removal of the endothelium or pretreatment of L-NNA, L-NAME, MB, ODQ, nifedipine and verapamil, but not by pretreatment of etrabutylammonium and glibenclamide. These findings suggest that the vasorelaxant effect of fluoxetine is modulated by intracellular $Ca^{2+}$ with an involvement of endothelial NO-cGMP pathway and also may be related to the inhibition of $Ca^{2+}$ entry through voltage-gated channel.

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