This study assessed the effects of essential oil of Foeniculum vulgare Mill. (fennel oil) and of trans- anethole, the main component of fennel oil, on extracellular Ca ²⁺ -induced store-operated Ca ²⁺ entry (SOCE) into vascular endothelial (EA) cells and their mechanisms of action. Components of fennel oil were analyzed by gas chromatography-mass spectrometry. Cytosolic Ca ²⁺ concentration ([Ca ²⁺ ] _c ) in EA cells was determined using Fura-2 fluorescence. In the presence of extracellular Ca ²⁺ , fennel oil significantly increased [Ca ²⁺ ] _c in EA cells; this increase was significantly inhibited by the Ca ²⁺ channel blockers La ³⁺ and nifedipine. In contrast, fennel oil induced [Ca ²⁺ ] _c was significantly lower in Ca ²⁺ -free solution, suggesting that fennel oil increases [Ca ²⁺ ] _c mainly by enhancing Ca ²⁺ influx into EA cells. [Ca ²⁺ ] _c mobilization by trans- anethole was similar to that of fennel oil. Moreover, SOCE was suppressed by fennel oil and trans- anethole. SOCE was also attenuated by lanthanum (La ³⁺ ), a non-selective cation channel (NSC) blocker; 2-aminoethoxydiphenyl borane (2-APB), an inositol 1,4,5-triphosphate (IP ₃ ) receptor inhibitor and SOCE blocker; and U73122, an inhibitor of phospholipase C (PLC). Further, SOCE was more strongly inhibited by La ³⁺ plus fennel oil or trans- anethole than by La ³⁺ alone. These findings suggest that fennel oil and trans- anethole significantly inhibit SOCE-induced [Ca ²⁺ ] _c increase in vascular endothelial cells and that these reactions may be mediated by NSC, IP ₃ –dependent Ca ²⁺ mobilization, and PLC activation.