Endothelium-dependent vasodilator effect of Euterpe oleracea Mart. (Açaí) extracts in mesenteric vascular bed of the rat

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• 作者：A. P.M. Rocha ; L.C.R.M. Carvalho ; M.A.V. Sousa ; S.V.F. Madeira ; P.J.C. Sousa ; T. Tano ; V.B. Schini-Kerth ; A.C. Resende ; R. Soares de Moura
• 关键词：Aç ; ai ; Euterpe oleracea Mart ; Vasodilation ; EDHF ; NO
• 刊名：Vascular Pharmacology
• 出版年：2007
• 期刊代码：59_15371891
• 类别：pha
• 出版时间：February 2007
• 卷：46
• 期：2
• 页码：97-104
• 文件大小：478 K

摘要

Açai (Euterpe oleracea Mart.) a fruit from the Amazon region, largely consumed in Brazil is rich in polyphenols. Experiments were undertaken to determine whether hydro-alcoholic extract obtained from stone of açaí induces a vasodilator effect in the rat mesenteric vascular bed precontracted with norepinephrine (NE) and, if so, to elucidate the underlying mechanism. Açai stone extract (ASE, 0.3–100 μg) induced a long-lasting endothelium-dependent vasodilation that was significantly reduced by N^G-nitro-l-arginine methyl ester (l-NAME) and ¹H-[1,2,3] oxadiazolo [4,4-a] quinoxalin-l-one (ODQ) and abolished by KCl (45 mM) plus l-NAME. In vessels precontrated with NE and KCl (45 mM) or treated with K_Ca⁺² channel blockers (charybdotoxin plus apamin), the effect of ASE was significantly reduced. However this effect is not affect by indomethacin, glybenclamide and 4-aminopiridine. Atropine, pyrilamine, yohimbine and HOE 140 significantly reduced the vasodilator effect of acetylcholine, histamine, clonidine and bradykinin, respectively, but did not change the vasodilator effect of ASE. In cultured endothelial cells ASE (100 μg/mL) induced the formation of NO that was reduced by N^G-nitro-l-arginine (l-NA, 100 μM). The present study demonstrates that the vasodilator effect of ASE is dependent on activation of NO-cGMP pathway and may also involve endothelium-derived hyperpolarizing factor (EDHF) release. The vasodilator effect suggest a possibility to use ASE as a medicinal plant, in the treatment of cardiovascular diseases.