摘要
Objective:To studytheaorticremodelingproducedby chronicsinoaorticdenervation(SAD)anditstime course,andto studytheroleof humoralfactorintheSAD-inducedaorticremodeling.Methods:In ratswithchronicSAD or shamoperation,theaorticstructurewasmeasuredby computer-assistedimageanalysis,theaorticfunctionby isolated arterypreparation,andangiotensinⅡconcentrationby radioimmunoassay.Results and Conclusion:Theaorticstructural remodelingdevelopedprogressivelyat4,8,16and32weeksafterSAD.AorticstructuralremodelingafterSADexpressed mainlyas aortichypertrophydue to SMC growthand collagenaccumulation.The aorticcontractionelicitedby nore-pinephrine(NE)wasprogressivelyincreased8,16and32weeksafterSAD.Theaorticrelaxationelicitedby acetylcholine(ACh)wasdepressed8,16and32weeksafterSAD.Inaddition,in32-weekSADratstheNE-inducedcontractionwasnot increasedby endothelialdenudation.TheseindicatedthattheincreasedcontractionanddepressedrelaxationafterSAD wererelatedto thechangeof endotheliumand/orthechangeof interactionbetweenendotheliumandSMC.In10-week SADrats,plasmaangiotensinⅡconcentrationremainedunchanged,whereasaorticangiotensinⅡconcentrationwas sig-nificantlyincreased,suggestingthatactivationof tissuerenin-angiotensinsystemmaybe involvedin SAD-inducedaortic remodeling.
Objective:To studytheaorticremodelingproducedby chronicsinoaorticdenervation(SAD)anditstime course,andto studytheroleof humoralfactorintheSAD-inducedaorticremodeling.Methods:In ratswithchronicSAD or shamoperation,theaorticstructurewasmeasuredby computer-assistedimageanalysis,theaorticfunctionby isolated arterypreparation,andangiotensinⅡconcentrationby radioimmunoassay.Results and Conclusion:Theaorticstructural remodelingdevelopedprogressivelyat4,8,16and32weeksafterSAD.AorticstructuralremodelingafterSADexpressed mainlyas aortichypertrophydue to SMC growthand collagenaccumulation.The aorticcontractionelicitedby nore-pinephrine(NE)wasprogressivelyincreased8,16and32weeksafterSAD.Theaorticrelaxationelicitedby acetylcholine(ACh)wasdepressed8,16and32weeksafterSAD.Inaddition,in32-weekSADratstheNE-inducedcontractionwasnot increasedby endothelialdenudation.TheseindicatedthattheincreasedcontractionanddepressedrelaxationafterSAD wererelatedto thechangeof endotheliumand/orthechangeof interactionbetweenendotheliumandSMC.In10-week SADrats,plasmaangiotensinⅡconcentrationremainedunchanged,whereasaorticangiotensinⅡconcentrationwas sig-nificantlyincreased,suggestingthatactivationof tissuerenin-angiotensinsystemmaybe involvedin SAD-inducedaortic remodeling.
基金
SupportedbytheNationalNaturalScienceFoundationofChina(No.39670831
30070871).
