Objective: To investigated the effects and mechanism of salvianolic acid B (Sal B) on vasorelaxation of isolated thoracic aorta in rats. Method: SD rats were used to establish isolated thoracic aorta perfusion models

and the cumulative dosing method was used to add Sal B to make final concentrations of 1×10-8

1×10-7

1×10-6

1×10-5

1×10-4 mol·L-1. The vascular tension changes were observed

and the effects 1×10-5

1×10-4 mol·L-1 Sal B on the constriction of norepinephrine (NE) and KCl preconstricted thoracic aorta were observed in rats. Result: The effect of Sal B on the basal tonus in isolated aortic rings in rats with endothelial integrity or endothelial injury was not so significant. Sal B dependently caused relaxation in vessels precontracted with NE but had no effect on KCl precontracted vessels. However

the relaxation effect of Sal B was not significantly inhibited by NG-nitro-L-arginine methylester (L-NAME) and Indomethacin (Indo). Also

the relaxation effect of Sal B was not significantly inhibited by tetraethylammonium (TEA)

4-aminopyridine (4-AP) and glibenclamide (Glib). The relaxation effect of Sal B was also not significantly inhibited by beta-blocker propranolol. But Sal B can inhibit the contraction vessels induced by extracellular calcium and intracellular calcium and its effect on latter is stronger than that on the former. Conclusion: The mechanisms may involve the reduction in Ca2+ influx through the receptor-dependent pathway

voltage-dependent pathway and blocking the IP3 receptor-induced Ca2+ release

but not correlated with NO-guanylyl cyclase pathway

COX pathway

K+ channels or β receptor.