ACE gene dosage determines additional autonomic dysfunction and increases renal angiotensin II levels in diabetic mice

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dc.contributor.authorde Moraes O.A.
dc.contributor.authorFlues K.
dc.contributor.authorScapini K.B.
dc.contributor.authorMostarda C.
dc.contributor.authorEvangelista F.S.
dc.contributor.authorRodrigues B.
dc.contributor.authorDartora D.R.
dc.contributor.authorFiorino P.
dc.contributor.authorAngelis K.D.
dc.contributor.authorIrigoyen M.C.
dc.date.accessioned2024-03-12T23:59:16Z
dc.date.available2024-03-12T23:59:16Z
dc.date.issued2018
dc.description.abstract© 2018 CLINICS.OBJECTIVES: The present study aimed to investigate cardiovascular autonomic modulation and angiotensin II (Ang II) activity in diabetic mice that were genetically engineered to harbor two or three copies of the angiotensin-converting enzyme gene. METHODS: Diabetic and non-diabetic mice harboring 2 or 3 copies of the angiotensin-converting enzyme gene were used in the present study. Animals were divided into 4 groups: diabetic groups with two and three copies of the angiotensin-converting enzyme gene (2CD and 3CD) and the respective age-matched non-diabetic groups (2C and 3C). Hemodynamic, cardiovascular, and autonomic parameters as well as renal Ang II expression were evaluated. RESULTS: Heart rate was lower in diabetic animals than in non-diabetic animals. Autonomic modulation analysis indicated that the 3CD group showed increased sympathetic modulation and decreased vagal modulation of heart rate variability, eliciting increased cardiac sympathovagal balance, compared with all the other groups. Concurrent diabetes and either angiotensin-converting enzyme polymorphism resulted in a significant increase in Ang II expression in the renal cortex. CONCLUSION: Data indicates that a small increase in angiotensin-converting enzyme activity in diabetic animals leads to greater impairment of autonomic function, as demonstrated by increased sympathetic modulation and reduced cardiac vagal modulation along with increased renal expression of Ang II.
dc.description.volume73
dc.identifier.doi10.6061/clinics/2018/e246
dc.identifier.issn1807-5932
dc.identifier.urihttps://dspace.mackenzie.br/handle/10899/35609
dc.relation.ispartofClinics
dc.rightsAcesso Aberto
dc.subject.otherlanguageAutonomic nervous system
dc.subject.otherlanguageMice
dc.subject.otherlanguageRenal angiotensin system
dc.subject.otherlanguageRenin-angiotensin system
dc.titleACE gene dosage determines additional autonomic dysfunction and increases renal angiotensin II levels in diabetic mice
dc.typeArtigo
local.scopus.citations3
local.scopus.eid2-s2.0-85051296115
local.scopus.subjectAngiotensin II
local.scopus.subjectAnimals
local.scopus.subjectAutonomic Nervous System
local.scopus.subjectBlood Glucose
local.scopus.subjectCardiovascular System
local.scopus.subjectDiabetes Mellitus, Experimental
local.scopus.subjectGene Dosage
local.scopus.subjectHeart Rate
local.scopus.subjectImmunohistochemistry
local.scopus.subjectKidney
local.scopus.subjectMale
local.scopus.subjectMice
local.scopus.subjectPeptidyl-Dipeptidase A
local.scopus.subjectPolymerase Chain Reaction
local.scopus.subjectRandom Allocation
local.scopus.subjectVagus Nerve
local.scopus.updated2024-05-01
local.scopus.urlhttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85051296115&origin=inward
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