Blood-brain barrier lesion-a novel determinant of autonomic imbalance in heart failure and the effects of exercise training

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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.authorRAQUEL, Hiviny de Ataides
dc.contributor.authorPEREGO, Sany M.
dc.contributor.authorMASSON, Gustavo S.
dc.contributor.authorJENSEN, Leonardo
dc.contributor.authorCOLQUHOUN, Alison
dc.contributor.authorMICHELINI, Lisete C.
dc.date.accessioned2023-10-30T14:40:42Z
dc.date.available2023-10-30T14:40:42Z
dc.date.issued2023
dc.description.abstractHeart failure (HF) is characterized by reduced ventricular function, compensatory activa-tion of neurohormonal mechanisms and marked autonomic imbalance. Exercise training (T) is effective to reduce neurohormonal activation but the mechanism underlying the au-tonomic dysfunction remains elusive. Knowing that blood-brain barrier (BBB) lesion con-tributes to autonomic imbalance, we sought now to investigate its involvement in HF-and exercise-induced changes of autonomic control. Wistar rats submitted to coronary artery ligation or SHAM surgery were assigned to T or sedentary (S) protocol for 8 weeks. After hemodynamic/autonomic recordings and evaluation of BBB permeability, brains were har-vesting for ultrastructural analysis of BBB constituents, measurement of vesicles trafficking and tight junction's (TJ) tightness across the BBB (transmission electron microscopy) and caveolin-1 and claudin-5 immunofluorescence within autonomic brain areas. HF-S rats ver-sus SHAM-S exhibited reduced blood pressure, augmented vasomotor sympathetic activity, increased pressure and reduced heart rate variability, and, depressed reflex sensitivity. HF-S also presented increased caveolin-1 expression, augmented vesicle trafficking and a weak TJ (reduced TJ extension/capillary border), which determined increased BBB permeability. In contrast, exercise restored BBB permeability, reduced caveolin-1 content, normalized vesicles counting/capillary, augmented claudin-5 expression, increased TJ tightness and selectivity simultaneously with the normalization of both blood pressure and autonomic bal-ance. Data indicate that BBB dysfunction within autonomic nuclei (increased transcytosis and weak TJ allowing entrance of plasma constituents into the brain parenchyma) underlies the autonomic imbalance in HF. Data also disclose that exercise training corrects both tran-scytosis and paracellular transport and improves autonomic control even in the persistence of cardiac dysfunction.eng
dc.description.indexMEDLINE
dc.description.indexPubMed
dc.description.indexWoS
dc.description.indexScopus
dc.description.sponsorshipFundac,auml;o de Amparo a Pesquisa do Estado de Sauml;o Paulo (FAPESP) [2018/14544-6, 2017/22156-3]
dc.description.sponsorshipConselho Nacional do Desenvolvimento Cienti'?co e Tecnolgico (CNPq) [304070/2019-0]
dc.identifier.citationCLINICAL SCIENCE, v.137, n.15, p.1049-1066, 2023
dc.identifier.doi10.1042/CS20230489
dc.identifier.eissn1470-8736
dc.identifier.issn0143-5221
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/56206
dc.language.isoeng
dc.publisherPORTLAND PRESS LTDeng
dc.relation.ispartofClinical Science
dc.rightsrestrictedAccesseng
dc.rights.holderCopyright PORTLAND PRESS LTDeng
dc.subject.othersympathetic-nerve activityeng
dc.subject.otherangiotensin-iieng
dc.subject.otherparaventricular nucleuseng
dc.subject.othernitric-oxideeng
dc.subject.othersystemeng
dc.subject.otherpermeabilityeng
dc.subject.otherbreakdowneng
dc.subject.othermechanismeng
dc.subject.othermfsd2aeng
dc.subject.wosMedicine, Research & Experimentaleng
dc.titleBlood-brain barrier lesion-a novel determinant of autonomic imbalance in heart failure and the effects of exercise trainingeng
dc.typearticleeng
dc.type.categoryoriginal articleeng
dc.type.versionpublishedVersioneng
dspace.entity.typePublication
hcfmusp.author.externalRAQUEL, Hiviny de Ataides:Univ Sao Paulo, Biomed Sci Inst, Dept Physiol & Biophys, Sao Paulo, SP, Brazil
hcfmusp.author.externalPEREGO, Sany M.:Univ Sao Paulo, Biomed Sci Inst, Dept Physiol & Biophys, Sao Paulo, SP, Brazil
hcfmusp.author.externalMASSON, Gustavo S.:Univ Sao Paulo, Biomed Sci Inst, Dept Physiol & Biophys, Sao Paulo, SP, Brazil
hcfmusp.author.externalCOLQUHOUN, Alison:Univ Sao Paulo, Biomed Sci Inst, Dept Cell Biol, Sao Paulo, SP, Brazil
hcfmusp.author.externalMICHELINI, Lisete C.:Univ Sao Paulo, Biomed Sci Inst, Dept Physiol & Biophys, Sao Paulo, SP, Brazil
hcfmusp.citation.scopus1
hcfmusp.contributor.author-fmusphcLEONARDO JENSEN SOCAS
hcfmusp.description.beginpage1049
hcfmusp.description.endpage1066
hcfmusp.description.issue15
hcfmusp.description.volume137
hcfmusp.origemWOS
hcfmusp.origem.pubmed37477956
hcfmusp.origem.scopus2-s2.0-85166387475
hcfmusp.origem.wosWOS:001046106300001
hcfmusp.publisher.cityLONDONeng
hcfmusp.publisher.countryENGLANDeng
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