Mechanisms involved in the endothelium-dependent vasodilatory effect of an ethyl acetate fraction of Mart. in isolated rats' aorta rings.

The species Mart. is a tree fern, commonly known as "xaxim", which is found in tropical and subtropical areas of Brazil. The present study investigated the mechanisms related with the vasorelaxant effects of an Ethyl Acetate Fraction (EAF) obtained from in rats' thoracic aorta rings. In pre-contracted vessels, EAF (0.1-1000 μg/mL) caused a concentration-dependent relaxation. The endothelium denudation, the nitric oxide (NO) synthase and guanylyl cyclase inhibitor reduced the vasodilation, indicating the participation of NO/cGMP pathway in its effect. The relaxation of EAF was abolished in the absence of extracellular Ca and was significantly decreased in the presence of Ca entry blocker, suggesting that Ca influx plays an important role in EAF effect and probably in eNOS activity. However, the PI3K/Akt pathway is not responsible for eNOS phosphorylation/activation. The vasodilator effect of EAF was partially inhibited by KCl 40 mM and almost totally abolished with L-NOARG + KCl 40 mM, indicating also the role of hyperpolarization in its effect. Calcium activated K channels are not involved in the EAF-induced hyperpolarization. The COX inhibitor, indomethacin, slightly reduced the vasodilation induced by EAF. In addition, EAF did not alter the relaxant effects of NO-donor, indicating that the relaxant activity cannot be attributed to free radical-scavenging properties. In conclusion, the present study showed that the EAF, causes an endothelium-dependent vasorelaxant effect in aorta that mainly involves the NO-cGMP pathway, hyperpolarization and prostanoids. The vasorelaxant activity of EAF can be attributed to the occurrence of polyphenol compounds.