Previous studies from our group have been demonstrated that myricitrin, a flavonoid that occur naturally and are widespread in higher plants, is able to inhibit nociceptive behaviour induced by acetic acid-induced visceral pain; glutamate, capsaicin and phorbol 12-myristate 13-aceta (PMA) induced licking behaviour and bradykinin-induced painful mechanical hypersensitivity. Myricitrin effects are attributed, mainly, to its properties on the protein kinase C and nitric oxide inhibition. Thus, the present study was designed to investigate the role of the K⁺ and Ca⁺² channels on the antinociceptive action of the myricitrin. Myricitrin (1mg/kg), given by intraperitoneal (i.p.) route, inhibited significantly (85±5%) the visceral pain caused by acetic acid (0.6%, i.p.) in mice. The glibenclamide (2 mg/kg, ATP-gated K⁺ channels blocker) i.p. pre-treatment prevented partially (45±12%), but significantly the myricitrin-induced antinociception. In addition, the antinociceptive effects of myricitrin and morphine (2.5 mg/kg) were completely prevented by intracerebroventricular (i.c.v.) injection of calcium chloride (CaCl₂). Calcium influx analysis (in vitro) revealed that myricitrin (100 and 200 µM) inhibited 46±13 and 48±11%, respectively, ⁴⁵Ca²⁺ influx under a K⁺-induced depolarizing condition; however, it inhibited (42±2%) calcium transport in a non-depolarizing condition just at the highest (200 µM) concentration used. In accordance with our previous findings, these results point out that myricitrin produces consistent antinociception in mice. The mechanisms investigated in this study become clear an involvement of ATP-gated K⁺ channels opening besides a reduction of the calcium influx on the myricitrin-induced antinociception.