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Aim To evaluate the vasorelaxant effects of the flavonone pinocembrin in isolated rat basilar artery rings and to investigate its possible mechanisms.Methods The isotonic contractions of the basilar artery tings from SD rats were recorded.Results Pinocembrin exerted vasorelaxation in a dosedependent manner in KCL (60 mmol ·L1) or 5HT (1 μmol · L1)induced sustained contraction and partial loss of the vasorelaxation in endotheliumdenuded rings.Pretreatment with pinocembrin (30 or 50 μmol · L1) attenuated contractile responses to KCl (10~60 mmol · L1) and 5HT (0.001 ~ 10 μmol · L1).The pinocembrininduced vasorelaxation was significantly reduced by the nitric oxide synthase inhibitor NωnitroLarginine methyl ester (LNAME, 100 μmol · L1),the guanylate cyclase inhibitor ODQ (5 μmol · L1) and the cyclooxygenase inhibitor indomethacin (5 μmol ·Lt).The voltagedependent K+ channel blocker 4aminopyridine (100 μmol · L1), the ATPsensitive K+channel blocker glibenclamide (10 μmol · L1) and Ca2 +activated K + channel blocker tetraethylammonium (1mmol · L1) remarkably attenuated pinocembrininduced relaxations.Pinocembrin also inhibited contraction induced by increasing external calcium in Ca2 +free medium plus 60 mmol · L1 KCl.Conclusion These results demonstrate that pinocembrin has a vasorelaxant effect on isolated rat basilar artery rings and may exert its action through an endotheliumdependent pathway, involving NOcGMP, and also through an endotheliumindependent pathway, opening K + channels and blockade of Ca2+ channels.