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

Acai (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 acai induces a vasodilator effect in the rat mesenteric vascular bed precontracted with norepinephrine (NE) and, if so, to elucidate the underlying mechanism. Acai stone extract (ASE, 0.3-100 mu g) induced a long-lasting endothelium-dependent vasodilation that was significantly reduced by N-G-nitro-L-arginine methyl ester (L-NAME) and H-1-[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 mu g/mL) induced the formation of NO that was reduced by N-G-nitro-L-arginine (L-NA, 100 mu M). 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. (c) 2006 Elsevier Inc. All rights reserved.