Objective: To observe vasodilation effect of baicalein (BAI) and its mechanism. Method: Isotonic tension was recorded in isolated rat thoracic artery induced by norepinephrine(NE

1×10-6mol·L-1) and KCl(6×10-2mol·L-1). To investigate the vasodilation effect of BAI and the influence of various drugs on it were observed in the rings with endothelium intact or endothelium denuded. Result: BAI was shown to significantly relax the endothelium-intact arteries induced by NE and KCl

relaxation had fall down on endothelium-denuded arteries. NG-nitro-L-argininemethylester (L-NAME

1×10-4mol·L-1)

methylene blue (MB

1×10-5mol·L-1)

tetrathylamonium(TEA

1×10-3mol·L-1)

4-aminopyridine (4-AP

1×10-4mol·L-1)

BaCl2(1×10-4mol·L-1) had no effect on the vasodilation of baicalein on thoracic aortas induced by NE

but indomethacin (INDO

1×10-5mol·L-1) and glibenclamide (1×10-5mol·L-1) did block the vascular effect of baicalein. In the absence of extracellular Ca2+ pre-incubation of the aortic rings with baicalein reduced significantly the contraction induced by NE. Conclusion: BAI can lead to a significantly relaxation in rat aortic rings. The effects are dependent on the concentrations

the role of endothelium-dependent and endothelium-independent characteristics. Moreover

prostaglandin(PGI2) pathway might be involved in the endothelium-dependent relaxation. The other mechanism was related to the inhibition of KATP channel

voltage-dependent Ca2+channel and receptors-operate Ca2+ channel.