简介：Objective:Tostudytheeffectofnitricoxide-inducedtyrosinephosphorylationoflarge-conductancecalcium-activatedpotassium(BKCa)channelαsubunitonvascularhyporesponsivenessinrats.Methods:Atotalof46Wistarratsofeithersex,weighing250g±20g,wereusedinthisstudy.Modelsofvascularhyporesponsivenessinducedbyhemorrhagicshock(30mmHgfor2hours)invivoandbyL-arginineinvitrowereestablishedrespectively.Thevascularresponsivenessofisolatedsuperiormesentericarteriestonorepinephrinewasobserved.TyrosinephosphorylationofBKCaαsubunitwasevaluatedwithmethodsofimmunoprecipitationandWesternblotting.Results:Inthesmoothmusclecellsofthesuperiormesentericarteries,theexpressionofBKCaαsubunittyrosinephosphorylationincreasedfollowinghemorrhagicshock,andL-argininecouldinduceBKCachannelαsubunittyrosinephosphorylationinatime-anddose-dependentmanner.L-NAME(Nω-nitro-L-arginine-methyl-ester),anitricoxidesynthetaseinhibitor,couldpartlyrestorethedecreasedvasoresponsivenessofthesuperiormesentericarteriesafterhemorrhagicshockinrats.Down-regulatingtheproteintyrosinephosphorylationwithgenistein,awidely-usedspecialproteintyrosinekinaseinhibitor,couldpartlyimprovethedecreasedvasoresponsivenessofthesuperiormesentericarteriesinducedbyL-arginineinvitro,whileup-regulatingtheproteintyrosinephosphorylationwithNa3VO4,aproteintyrosinephosphataseinhibitor,couldfurtherdecreasethenitricoxide-inducedvascularhyporesponsiveness,whichcouldbepartlyamelioratedby0.1mmol/Ltetrabutylammoniumchloride(TEA),aselectiveBKCainhibitoratthisconcentration.Conclusions:NitricoxidecaninducethetyrosinephosphorylationofBKCaαsubunit,whichinfluencesthevascularhyporesponsivenessinhemorrhagicshockratsorinducedbyL-arginineinvitro.