Sympatheticregulationofvascularfunctioninhealthanddisease

Abstract

Thesympatheticnervoussystem(SNS)isknowntoplayapivotalroleinshort-andlong-termregulationofdifferentfunctionsofthecardiovascularsystem.Inthepastdecadesincreasingevidencedemonstratedthatsympatheticneuralcontrolisinvolvednotonlyinthevasomotorcontrolofsmallresistanearteriesbutalsoinmodulationoflargearteryfunction.Sympatheticactivityandvascularfunction,bothofwhicharekeyfactorsinthedevelopmentandprognosisofcardiovasculareventsanddisease,arelinkedatseverallevels.EvidencefromexperimentalstudiesindicatesthattheSNSiscriticallyinfluenced,atthecentralandalsoattheperipherallevel,bythemostrelevantfactorsregulatingvascularfunction,suchasnitricoxide(NO),reactiveoxygenspecies(ROS),endothelin(ET),therenin-angiotensinsystem.Additionally,thereisindirectevidenceofareciprocalrelationshipbetweenendothelialfunctionandactivityoftheSNS.Anumberofcardiovascularriskfactorsanddiseasesarecharacterizedbothbyincreasedsympatheticoutflowanddecreasedendothelialfunction.Inhealthysubjects,musclesympatheticnerveactivity(MSNA)appearstoberelatedtosurrogatemarkersofendothelialfunction,andanacuteincreaseinsympatheticactivityhasbeenassociatedwithadecreaseinendothelialfunctioninhealthysubjects.However,directevidenceofacause-effectrelationshipfromhumanstudiesisscanty.Inhumanslargearterystiffnesshasbeenassociatedwithincreasedsympatheticdischarge,bothinhealthysubjectsandinrenaltransplantrecipients.Peripheralsympatheticdischargeisalsoabletomodulatewavereflection.Ontheotherhand,largearterystiffnesscaninterferewithautonomicregulationbyimpairingcarotidbaroreflexsensitivity