N-octanoyl-Dopamine Is an Agonist at the Capsaicin Receptor TRPV1 and Mitigates Is Chemia-Induced Acute Kidney Injury in Rat 英文参考文献.docVIP

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N-octanoyl-Dopamine Is an Agonist at the Capsaicin Receptor TRPV1 and Mitigates Is Chemia-Induced Acute Kidney Injury in Rat 英文参考文献.doc

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N-octanoyl-Dopamine Is an Agonist at the Capsaicin Receptor TRPV1 and Mitigates Is Chemia-Induced Acute Kidney Injury in Rat 英文参考文献

N-octanoyl-DopamineIsanAgonistattheCapsaicin ReceptorTRPV1andMitigatesIsChemia-InducedAcute KidneyInjuryinRat CharalambosTsagogiorgas1*,JohannesWedel2,MaximiliaHottenrott1,MichaelO.Schneider2, UtaBinzen3,WolfgangGreffrath3,Rolf-DetlefTreede3,BastianTheisinger4,SonjaTheisinger4, Ru¨digerWaldherr2,BernhardK.Kra¨mer2,ManfredThiel1,PeterSchnuelle2,BenitoA.Yard2, SimoneHoeger2 1DepartmentofAnaesthesiologyandIntensiveCareMedicine,UniversityMedicalCentreMannheim,MedicalFacultyMannheim,RuprechtKarlsUniversityHeidelberg, Mannheim, Germany, 2Department of Medicine V (Nephrology/Endocrinology/Rheumatology), University Medical Centre Mannheim, Medical Faculty Mannheim, RuprechtKarlsUniversityHeidelberg,Mannheim,Germany,3DivisionofNeurophysiology,CenterofBiomedicineandMedicalTechnologyMannheim(CBTM),Medical FacultyMannheim,RuprechtKarlsUniversityHeidelberg,Mannheim,Germany,4NovaliqGmbH,Heidelberg,Germany Abstract Since stimulation of transient receptor potential channels of the vanilloid receptor subtype 1 (TRPV1) mitigates acute kidney injury (AKI) and endogenous N-acyl dopamine derivatives are able to activate TRPV1, we tested if synthetic N- octanoyl-dopamine (NOD) activates TRPV1 and if it improves AKI. These properties of NOD and its intrinsic anti- inflammatorycharacterwerecomparedwiththoseofdopamine(DA).TRPV1activationandanti-inflammatory properties of NOD and DA were tested using primary cell cultures invitro. The influence of NOD and DA on AKI was tested in a prospective, randomized, controlled animal studywith42inbred maleLewisrats(LEW, RT1), treated intravenously with equimolar concentrations of DA or NOD one hour before the onset of warm ischemia and immediately before clamp release.NOD,butnotDA,activatesTRPV1channelsinisolateddorsalrootganglionneurons(DRG)thatinnervateseveral tissuesincludingkidney.InTNFastimulatedproximaltubularepithelialcells,inhibitionofNFkBandsubsequentinhibition ofVCAM1expressionbyNODwassignificantlystrongerthanbyDA.NODimprovedrenalfun