It has been reported that gallic acid induced vasocontraction and vasorelaxation. However, the effects of ester compound of gallic acid in vasoconstriction remain unclear. This study investigated the mechanism of vasorelaxation induced by propyl gallate (PG) in the endothelium-intact (E (+) ) and -denuded (E (-)) rat aorta. 1) PG phenylephrine (PE)-induced contraction in a dose-dependent manner on the E (+) and E (-) rat aorta. However, this inhibitory effect was stronger in E (+) aorta than that in E(-) aorta. 2) 4-aminopylidine, apamin or SQ22536 significantly recovered PG-evoked PE-induced contraction in E (-) aorta. 3) PG induced increases cAMP levels in E(-) aorta. 4) Pretreatment with L-NAME, but not indomethacin, significantly reduced PG-evoked E (+)-dependent vasorelaxation. 5) PG induced increases of eNOS phosphorylation in HUVECs. Pretreatment with Akti-1/2, a Akt inhibitor, or LY294002, PI3K inhibitor, but not PP2, Src inhibitor, significantly reduced PG-evoked eNOS phosphorylation. In conclusion, these results suggested that PG-induced endothelium-independent vasorelaxation partly related to activating K+ channel and/or cAMP pathway. Moreover, PG-induced endothelium-dependent vasorelaxation related to NO release from endothelium by activating eNOS via PI3K/Akt signal pathway.