Estudo do mecanismo vasorrelaxante do extrato etanólico e frações, das folhas de Echinodorus grandiflorus (Cham. & Schltdl.) Micheli, em leitos mesentéricos isolados

Abstract

Echinodorus grandiflorus (Cham. & Schltdl.) Micheli (Alismataceae) has been used as an antihypertensive and diuretic agent by several Brazilian native populations. However, the secondary metabolites responsible for this activity, as well as the molecular mechanisms responsible for its effects on peripheral vascular resistance remain unknown. The aim of this study was to evaluate the vasodilator and antioxidant effects of the ethanolic extract of the leaves of E. grandiflorus and hexane (HexFr), chloroform (ChlFr) and n-butanolic fractions (ButFr) in isolated perfused mesenteric beds. Initially, the ethanolic extract was obtained from E. grandiflorus leaves (EEEG), followed by liquid-liquid fractionation and high-performance liquid chromatography analysis of the obtained preparations. EEEG and ButFr showed a significant concentration of phenolic compounds and flavonoids with values significantly higher than those found in HexFr and ChlFr fractions. These compounds were identified as caffeic acid, p-coumaric acid, ferrulic acid and luteolin Subsequently, the vasodilating effects of EEEG and hexane, chloroform and n-butanolic fractions were evaluated in the beds and the preparation with the best effect was used for analyzes of in vitro mechanism in the beds. ButFr reduced the perfusion pressure in concentration-dependent isolated mesenteric beds. The removal or inhibition of endothelial nitric oxide and prostaglandin synthase by L-NAME associated with indomethacin inhibited the vasodilatory effects induced by EEEG and ButFr. In addition, the combination of atropine and HOE-140 completely inhibited EEEG and ButFrinduced vasodilation. Infusion with nutrient solution containing 40 mM KCl inhibited the vasodilator effect of all EEEG and ButFr doses. Finally, treatment with tetraethylammonium completely blocked EEG or ButFr induced vasodilation. This study showed that EEEG and ButFr have important vasodilatory effects on the mesenteric arterial beds. Apparently, these effects are dependent on the endothelial and B2 bradykininergic M3 muscarinic receptors, inducing the release of nitric oxide and prostacyclin, followed by activation of the sodium and potassium channels in vascular smooth muscle. This study opens perspectives for the use of EEEG or ButFr in situations where the reduction of perfusion pressure is necessary.