Abstract: Objective: Sodium aescinate (SA) is used as a vasoactive drug in clinical treatment. This study was designed to investigate the effects of SA on rat isolated thoracic aorta and the possible mechanisms. Methods: Isometric tension was recorded in response to drugs in organ bath. Results: The effects of SA obeyed an all-or-nothing response. SA in relatively low dose (≥50 μg/ml) had an endothelium-independent contractile effect in rat aorta (P <0.01), which depended on extracellular Ca2+ influx via L-type Ca2+ channel (P <0.05). SA in relatively high dose (≥100 μg/ml) also induced vasoconstriction in Ca2+-free medium (P <0.01), which was independent of the activity of inositol-1,4,5-trisphosphate receptor (IP3R), ryanodine receptor (RYR), and protein kinase C (PKC). SA in relatively high dose (≥100 μg/ml) dilated both endothelium-intact and endothelium-denuded aortic rings precontracted by phenylephrine (PE) or KCl (each P <0.01). SA inhibited extracellular Ca2+ influx induced by PE or KCl (each P <0.01) and had no activation effect on K+ channels on vascular smooth muscle. The relaxant effect of SA partly depended on the activity of NO synthase but not on the activity of cyclooxygenase. Conclusions: Taken together, this study indicated that SA had dual effects on vascular tension in rat isolated thoracic aorta. [Copyright &y& Elsevier]