BackgroundRecentstudieshaveshowedthatperivascularadiposetissue(PVAT)maysecretetheadventitial-derivedrelaxingfactor(ADRF)toaffectvascularfunction.However,thefunctionalchangeofADRFinhypertensivestatusisseldomstudied;andthemechanismsofADRFremainunclear.OurstudyexaminedtheADRFsecretedbyperivascularadiposetissueofcontrolratswithnormalbloodpressure(WistarKyotorats,WKY)anddiscussedthemechanismsofADRF;WeobservedthefunctionalchangeinADRFofperivascularadiposetissueinspontaneouslyhypertensiverats(SHRs).MethodThetwoadjacentthoracicaortaringsofSHRandWKYratswerepidedintonakedvesselsubgroupandPVATsubgroup.Thedifferencesofvascularcontractilitybetweenthetwosubgroupsinducedby10-6mmol/Lphenylephrinewerecompared.TheeffectofPVATculturemediumofWKYonthevasculartensionofFat(-)vesselswasobservedbyliquidtransfermeasure.ThemechanismofADRFwasdeterminedbytooldrugs.ResultsInWKYgroup,vascularcontractilityofFat(+)subgroupwaslowerthanthatoftheFat(-)subgroup(P<0.05);whileinSHRgroup,therewasnodifferencebetweenthetwosubgroups(P>0.05).TransferringtheincubationsolutionofWKYFat(+)subgrouptothematchedFat(-)subgroupinducedrapidvasodilation.WhenincubatingbloodvesselsincalciumfreePSSsolution,therewasnosignificantdifferenceofphenylephrine-inducedvasoconstrictionbetweenFat(-)andFat(+)subgroup.Bothglibenclamide,theblockerofATP-sensitivepotassium(KATP)channelandTetraethy-lammoniumchloride(TEA),theinhibitorofcalcium-dependentpotassium(KCa)channel,effectivelyinhibitedvasodilationfunctionofADRF.ConclusionsPerivascularadiposetissueinWKYreleasesADRFwhichcancausevasodilation,whilethisfunctionwasinhibitedinSHR.ADRFactsthroughtheactivationofKCaandKATPchannelsandcalciumionisinvolved.
