Rocha A P M, Carvalho L C R M, Sousa M A V, Madeira S V F, Sousa P J C, Tano T, Schini-Kerth V B, Resende A C, Soares de Moura R
Department of Pharmacology and Psychobiology, IBRAG, UERJ, Rio de Janeiro, Brazil.
Vascul Pharmacol. 2007 Feb;46(2):97-104. doi: 10.1016/j.vph.2006.08.411. Epub 2006 Sep 1.
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 microg) induced a long-lasting endothelium-dependent vasodilation that was significantly reduced by N(G)-nitro-l-arginine methyl ester (l-NAME) and (1)H-[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 microg/mL) induced the formation of NO that was reduced by N(G)-nitro-l-arginine (l-NA, 100 microM). 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.
阿萨伊果（Euterpe oleracea Mart.）是一种来自亚马逊地区的水果，在巴西被大量食用，富含多酚。进行了实验以确定从阿萨伊果核中获得的水醇提取物是否能在去甲肾上腺素（NE）预收缩的大鼠肠系膜血管床中诱导血管舒张作用，如果是，则阐明其潜在机制。阿萨伊果核提取物（ASE，0.3 - 100微克）诱导了持久的内皮依赖性血管舒张，N(G)-硝基-L-精氨酸甲酯（L-NAME）和（1）H-[1,2,3]恶二唑并[4,4-a]喹喔啉-1-酮（ODQ）可显著降低该作用，而氯化钾（45毫摩尔）加L-NAME可消除该作用。在与NE和氯化钾（45毫摩尔）预收缩的血管中或用钾通道阻滞剂（蝎毒素加蜂毒明肽）处理的血管中，ASE的作用显著降低。然而，吲哚美辛、格列本脲和4-氨基吡啶不影响该作用。阿托品、吡拉明、育亨宾和HOE 140分别显著降低了乙酰胆碱、组胺、可乐定和缓激肽的血管舒张作用，但未改变ASE的血管舒张作用。在培养的内皮细胞中，ASE（100微克/毫升）诱导了一氧化氮的形成，N(G)-硝基-L-精氨酸（L-NA，100微摩尔）可降低该形成。本研究表明，ASE的血管舒张作用依赖于一氧化氮-环鸟苷酸途径的激活，也可能涉及内皮衍生超极化因子（EDHF）的释放。这种血管舒张作用提示了将ASE用作药用植物治疗心血管疾病的可能性。
