Baroreflex deficiency induces additional impairment of vagal tone, diastolic function and calcium handling proteins after myocardial infarction

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorMOSTARDA, Cristiano
dc.contributor.authorRODRIGUES, Bruno
dc.contributor.authorMEDEIROS, Alessandra
dc.contributor.authorMOREIRA, Edson D.
dc.contributor.authorMORAES-SILVA, Ivana C.
dc.contributor.authorBRUM, Patricia C.
dc.contributor.authorANGELIS, Katia De
dc.contributor.authorIRIGOYEN, Maria-Claudia
dc.date.accessioned2014-09-30T15:18:57Z
dc.date.available2014-09-30T15:18:57Z
dc.date.issued2014
dc.description.abstractBaroreflex dysfunction has been considered an important mortality predictor after myocardial infarction (MI). However, the impact of baroreflex deficiency prior to MI on tonic autonomic control and cardiac function, and on the profile of proteins associated with intracellular calcium handling has not yet been studied. The aim of the present study was to analyze how the impairment of baroreflex induced by sinoaortic denervation (SAD) prior to MI in rats affects the tonic autonomic control, ventricular function and cardiomyocyte calcium handling proteins. After 15 days of following or SAD surgery, rats underwent MI. Echocardiographic, hemodynamic, autonomic and molecular evaluations were performed 90 days after MI. Baroreflex impairment led to additional damage on: left ventricular remodeling, diastolic function, vagal tonus and intrinsic heart rate after MI. The loss of vagal component of the arterial baroreflex and vagal tonus were correlated with changes in the cardiac proteins involved in intracellular calcium homeostasis. Furthermore, additional increase in sodium calcium exchanger expression levels was associated with impaired diastolic function in experimental animals. Our findings strongly suggest that previous arterial baroreflex deficiency may induce additional impairment of vagal tonus, which was associated with calcium handling proteins abnormalities, probably triggering ventricular diastolic dysfunction after MI in rats.
dc.description.indexPubMed
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo [FAPESP-2007/58942-0, 2012/20141-5]
dc.description.sponsorshipConselho Nacional de Pesquisa e Desenvolvimento [CNPq-482520/2009-4, 306011/2010-7, 47-9766/2011-8]
dc.description.sponsorshipConselho Nacional de Pesquisa e Desenvolvimento (CNPq-BPQ)
dc.identifier.citationAMERICAN JOURNAL OF TRANSLATIONAL RESEARCH, v.6, n.3, p.320-328, 2014
dc.identifier.issn1943-8141
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/7972
dc.language.isoeng
dc.publisherE-CENTURY PUBLISHING CORP
dc.relation.ispartofAmerican Journal of Translational Research
dc.rightsopenAccess
dc.rights.holderCopyright E-CENTURY PUBLISHING CORP
dc.subjectArterial baroreflex
dc.subjectmyocardial infarction
dc.subjectautonomic tone
dc.subjectcardiac function
dc.subjectcardiac remodeling
dc.subjectcalcium handling proteins
dc.subject.otherfailing human myocardium
dc.subject.otherheart-rate-variability
dc.subject.otherhypertensive-rats
dc.subject.othersinoaortic denervation
dc.subject.otherautonomic function
dc.subject.otherdiabetes-mellitus
dc.subject.othersensitivity
dc.subject.othermortality
dc.subject.otherfailure
dc.subject.otherdysfunction
dc.subject.wosOncology
dc.subject.wosMedicine, Research & Experimental
dc.titleBaroreflex deficiency induces additional impairment of vagal tone, diastolic function and calcium handling proteins after myocardial infarction
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.author.externalMOSTARDA, Cristiano:Fed Univ Maranhao UFMA, Sao Luis, Maranhao, Brazil
hcfmusp.author.externalRODRIGUES, Bruno:Sao Judas Tadeu Univ USJT, Human Movement Lab, Sao Paulo, Brazil
hcfmusp.author.externalMEDEIROS, Alessandra:Fed Univ Sao Paulo UNIFESP, Sao Paulo, Brazil
hcfmusp.author.externalMORAES-SILVA, Ivana C.:Univ Sao Paulo, Sch Med, Heart Intitute InCor, Hypertens Unit, Sao Paulo, Brazil
hcfmusp.author.externalBRUM, Patricia C.:Univ Sao Paulo, Sch Phys Educ & Sports, Sao Paulo, Brazil
hcfmusp.author.externalANGELIS, Katia De:Nove de Julho Univ UNINOVE, Translat Physiol Lab, Sao Paulo, Brazil
hcfmusp.citation.scopus9
hcfmusp.contributor.author-fmusphcEDSON DIAS MOREIRA
hcfmusp.contributor.author-fmusphcMARIA CLAUDIA COSTA IRIGOYEN
hcfmusp.description.beginpage320
hcfmusp.description.endpage328
hcfmusp.description.issue3
hcfmusp.description.volume6
hcfmusp.origemWOS
hcfmusp.origem.pubmed24936224
hcfmusp.origem.scopus2-s2.0-84901065429
hcfmusp.origem.wosWOS:000338439400012
hcfmusp.publisher.cityMADISON
hcfmusp.publisher.countryUSA
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hcfmusp.remissive.sponsorshipCNPq
hcfmusp.remissive.sponsorshipFAPESP
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