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Objective:Tyrosine kinase inhibitors may be useful in the management of cerebral vasospasm. It has not yet reported whether potassium channel plays a role in tyrosine kinase inhibitors-induced vascular relaxation of cerebral artery. This study is undertaken to clarify the role of potassium channel in tyrosine kinase inhibitors-induced vascular relaxation, and to investigate the effect of tyrosine kinase inhibitors on outward potassium currents in freshly isolated smooth muscle cells from rat basilar artery. Methods:The isolation of rat basilar smooth muscle cells was performed by special techniques. The whole cell currents were recoreded by whole cell patch clamp technique in freshly isolated smooth muscle cells from rat basilar artery. Results:In present study, genistein(n=10), tyrphostin A-23(n=10), A-25(n=10) 30μM into bath solution increased the amplitude of the outward K+ current which was completely blocked by large conductance calcium-activated potassium channel(BKCa) blocker, iberiotoxin(0.1μM), and calcium chelator, BAPTA, in whole cell mode. In contrast, diadzein 30μM(n=10), inactive analogue of genistein, did not increase the amplitude of the outward K+ current. Conclusion:Our results suggest tyrosine kinase inhibitors such as genistein, tyrphostin A-23 and A-25 increase the BKCa channel activity in cerebral basilar smooth muscle cells, thereby contributing to the relaxation of cerebral artery. Key words:Vasospasm;Genistein;Tyrphostin A-23, A-25;Large conductance calcium-activated potassium channel;Patch clamp.