Abstract
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. Isometric tension was recorded in response to drugs in organ bath. The effects of SA obeyed an all-or-nothing response. SA in relatively low dose (> or = 50 microg/ml) had an endothelium-independent contractile effect in rat aorta (P<0.01), which depended on extracellular Ca(2+) influx via L-type Ca(2+) channel (P<0.05). SA in relatively high dose (> or = 100 microg/ml) also induced vasoconstriction in Ca(2+)-free medium (P<0.01), which was independent of the activity of inositol-1,4,5-trisphosphate receptor (IP(3)R), ryanodine receptor (RYR), and protein kinase C (PKC). SA in relatively high dose (> or = 100 microg/ml) dilated both endothelium-intact and endothelium-denuded aortic rings precontracted by phenylephrine (PE) or KCl (each P<0.01). SA inhibited extracellular Ca(2+) 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. Taken together, this study indicated that SA had dual effects on vascular tension in rat isolated thoracic aorta.
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