Angiotensin-(1–7) in Paraventricular Nucleus Modulates Sympathetic Activity and Cardiac Sympathetic Afferent Reflex in Renovascular Hypertensive Rats 英文参考文献.docVIP

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Angiotensin-(1–7) in Paraventricular Nucleus Modulates Sympathetic Activity and Cardiac Sympathetic Afferent Reflex in Renovascular Hypertensive Rats 英文参考文献.doc

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Angiotensin-(1–7) in Paraventricular Nucleus Modulates Sympathetic Activity and Cardiac Sympathetic Afferent Reflex in Renovascular Hypertensive Rats 英文参考文献

Angiotensin-(1–7)inParaventricularNucleusModulates SympatheticActivityandCardiacSympatheticAfferent ReflexinRenovascularHypertensiveRats YingHan,Hai-JianSun,PengLi,QingGao,Ye-boZhou,FengZhang,Xing-YaGao,Guo-QingZhu* KeyLaboratoryofCardiovascularDiseaseandMolecularIntervention,DepartmentofPhysiology,NanjingMedicalUniversity,Nanjing,Jiangsu,China Abstract Background: Excessive sympathetic activitycontributes tothepathogenesis andprogression ofhypertension. Enhanced cardiacsympatheticafferentreflex(CSAR)isinvolvedinsympatheticactivation.Thisstudywasdesignedtodeterminethe rolesofangiotensin(Ang)-(1–7)inparaventricularnucleus(PVN)inmodulatingsympatheticactivityandCSARanditssignal pathwayinrenovascularhypertension. Methodology/Principal Findings: Renovascular hypertension was induced with two-kidney, one-clip method. Renal sympatheticnerveactivity(RSNA)andmeanarterialpressure(MAP)wererecordedinsinoaortic-denervatedandcervical- vagotomized rats with anesthesia. CSAR was evaluated with the RSNA and MAP responses to epicardial application of capsaicin.PVNmicroinjectionofAng-(1–7)andcAMPanaloguedb-cAMPcausedgreaterincreasesinRSNAandMAP,and enhancement in CSAR in hypertensive rats than in sham-operated rats, while Mas receptor antagonist A-779 produced oppositeeffects.Therewasnosignificantdifferenceintheangiotensin-convertingenzyme2(ACE2)activityandAng-(1–7) levelinthePVNbetweensham-operatedratsandhypertensiverats,buttheMasreceptorproteinexpressioninthePVNwas increased in hypertensive rats. The effects of Ang-(1–7) were abolished by A-779, adenylyl cyclase inhibitor SQ22536 or protein kinase A (PKA) inhibitor Rp-cAMP. SQ22536 or Rp-cAMP reduced RSNA and MAP in hypertensive rats, and attenuatedtheCSARinbothsham-operatedandhypertensiverats. Conclusions:Ang-(1–7)inthePVNincreasesRSNAandMAPandenhancestheCSAR,whichismediatedbyMasreceptors. Endogenous Ang-(1–7) and Mas receptors contribute to the enhanced sympathetic outflow and CSAR in renovascular hypertension.AcAMP-PKApathwayisin