Abstract

The aim of this work was to characterize the vasorelaxant effect produced by Sida santaremnensis ethanol extract (Ssan-EtOH) in rat superior mesenteric artery. Ssan-EtOH showed neither acute toxicity nor hemolytic activity. In the other hand, it induced a concentration-dependent vasorelaxant effect on phenylephrine (10 μmol/L) or KCl (80 mmol/L)-induced pre-contractions in endothelium-intact rat mesenteric artery rings, which attenuated after endothelium removal, without changes in maximum effect. N^G-nitro-L-arginine methyl ester (L-NAME) (100 μmol/L), indomethacin (10 µmol/L), atropine (1 nmol/L), KCl (20 mmol/L) or tetraethylammonium (3 mmol/L) pretreatment also induced a response attenuation. The endothelium-derived hyperpolarizing factor (EDHF) involvement in Ssan-EtOH-induced vasorelaxant response was verified after L-NAME (100 μmol/L) plus Indomethacin (10 μmol/L) plus tetraethylammonium (3 mmol/L) pretreatment and this vasorelaxation was decreased. In endothelium-denuded rings, Ssan-EtOH was able to inhibit phenylephrine-induced contractions (10^-9 to 10^-5 mol/L) in a concentration-dependent manner. In a nominally without Ca²⁺ depolarizing Tyrode solution, Ssan-EtOH inhibited CaCl₂ (10^-6 – 3 x 10^-2 mol/L)-induced contractions in a concentration-dependent manner. The endothelium-dependent Ssan-EtOH-induced vasorelaxant effect probably involves the participation of the nitric oxide synthase (NOS) and cyclooxygenases (COX) pathways, as well muscarinic receptors and EDHF and the endothelium-independent effect probably occurs by Ca²⁺ influx inhibition through voltage-operated calcium channels.

Key words: Sida santaremnensis, superior mesenteric artery, Malvaceae, vasorelaxation.

Abbreviation

Ssan-EtOH, ethanol extract from aerial parts of Sida santaremnensis H. Monteiro; LD₅₀, lethal dose that induced 50% from death.