The Role of beta-Adrenergic Overstimulation in the Early Stages of Renal Injury

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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.authorPONTE, Mariana Charleaux de
dc.contributor.authorCASARE, Fernando Augusto Malavazzi
dc.contributor.authorCOSTA-PESSOA, Juliana Martins
dc.contributor.authorCARDOSO, Vanessa Gerolde
dc.contributor.authorMALNIC, Gerhard
dc.contributor.authorMELLO-AIRES, Margarida
dc.contributor.authorVOLPINI, Rildo Aparecido
dc.contributor.authorTHIEME, Karina
dc.contributor.authorOLIVEIRA-SOUZA, Maria
dc.date.accessioned2018-03-06T15:26:28Z
dc.date.available2018-03-06T15:26:28Z
dc.date.issued2017
dc.description.abstractBackground/Aims: To assess the possible contribution of the beta-adrenergic overstimulation in early stages of renal injury, the present study evaluated, in rats, the effects of the beta-adrenoceptor agonist isoproterenol (ISO) on renal function and morphology, as well as the renal mRNA and protein expression of the NADPH oxidase isoform 4 (Nox 4) and subunit p22(phox), endoplasmic reticulum (ER) stress, pro-inflammatory, pro-apoptotic and renin-angiotensin system (RAS) components. Methods: Wistar rats received ISO (0.3 mg.kg(-1).day(-1) s.c.) or vehicle (control) for eight days. At the end of the treatment, food and water intake, urine output and body weight gain were evaluated and renal function studies were performed. Renal tissue was used for the morphological, quantitative PCR and immunohistochemical studies. Results: ISO did not change metabolic parameters or urine output. However it induced a decrease in renal blood flow and an increase in the filtration fraction. These changes were accompanied by increased cortical mRNA and protein expression for the renal oxidative stress components including Nox 4 and p22(phox); ER stress, pro-inflamatory, pro-apoptotic as well as RAS components. ISO also induced a significant increase in medullar renin protein expression. Conclusion: These findings support relevant information regarding the contribution of specific beta-adrenergic hyperactivity in early stage of renal injury, indicating the reactive oxygen species, ER stress and intrarenal RAS as important factors in this process. (c) 2017 The Author(s) Published by S. Karger AG, Basel
dc.description.indexMEDLINE
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [13/195693]
dc.description.sponsorshipGerhard Malnic and Margarida de Mello-Aires [13/23087-4]
dc.description.sponsorshipFernando Augusto Malavazzi Casare [11/14022-0]
dc.description.sponsorshipVanessa Gerolde Cardoso [14/19154-0]
dc.description.sponsorshipKarina Thieme [14/17251-9]
dc.description.sponsorshipConselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [14/151575-2]
dc.identifier.citationKIDNEY & BLOOD PRESSURE RESEARCH, v.42, n.6, p.1277-1289, 2017
dc.identifier.doi10.1159/000485931
dc.identifier.eissn1423-0143
dc.identifier.issn1420-4096
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/25840
dc.language.isoeng
dc.publisherKARGER
dc.relation.ispartofKidney & Blood Pressure Research
dc.rightsopenAccess
dc.rights.holderCopyright KARGER
dc.subjectIsoproterenol
dc.subjectbeta-adrenergic stimulation
dc.subjectRenal hemodynamics
dc.subjectOxidative stress
dc.subjectInflammation
dc.subjectIntrarenal renin-angiotensin system
dc.subject.otherendoplasmic-reticulum stress
dc.subject.otheradult cardiac myocytes
dc.subject.otherfactor-kappa-b
dc.subject.otherangiotensin-ii
dc.subject.otherneural-control
dc.subject.otherconverting-enzyme
dc.subject.othergene-expression
dc.subject.otherdisease
dc.subject.otherkidney
dc.subject.otherrat
dc.subject.wosPhysiology
dc.subject.wosUrology & Nephrology
dc.subject.wosPeripheral Vascular Disease
dc.titleThe Role of beta-Adrenergic Overstimulation in the Early Stages of Renal Injury
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.author.externalPONTE, Mariana Charleaux de:Univ Sao Paulo, Dept Physiol & Biophys, Lab Renal Physiol, Inst Biomed Sci,Med Sch, Sao Paulo, Brazil
hcfmusp.author.externalCASARE, Fernando Augusto Malavazzi:Univ Sao Paulo, Dept Physiol & Biophys, Lab Renal Physiol, Inst Biomed Sci,Med Sch, Sao Paulo, Brazil
hcfmusp.author.externalCOSTA-PESSOA, Juliana Martins:Univ Sao Paulo, Dept Physiol & Biophys, Lab Renal Physiol, Inst Biomed Sci,Med Sch, Sao Paulo, Brazil
hcfmusp.author.externalCARDOSO, Vanessa Gerolde:Univ Sao Paulo, Dept Physiol & Biophys, Lab Renal Physiol, Inst Biomed Sci,Med Sch, Sao Paulo, Brazil
hcfmusp.author.externalMALNIC, Gerhard:Univ Sao Paulo, Dept Physiol & Biophys, Lab Renal Physiol, Inst Biomed Sci,Med Sch, Sao Paulo, Brazil
hcfmusp.author.externalMELLO-AIRES, Margarida:Univ Sao Paulo, Dept Physiol & Biophys, Lab Renal Physiol, Inst Biomed Sci,Med Sch, Sao Paulo, Brazil
hcfmusp.author.externalOLIVEIRA-SOUZA, Maria:Univ Sao Paulo, Dept Physiol & Biophys, Lab Renal Physiol, Inst Biomed Sci,Med Sch, Sao Paulo, Brazil
hcfmusp.citation.scopus14
hcfmusp.contributor.author-fmusphcRILDO APARECIDO VOLPINI
hcfmusp.contributor.author-fmusphcKARINA THIEME
hcfmusp.description.beginpage1277
hcfmusp.description.endpage1289
hcfmusp.description.issue6
hcfmusp.description.volume42
hcfmusp.origemWOS
hcfmusp.origem.pubmed29262407
hcfmusp.origem.scopus2-s2.0-85048358078
hcfmusp.origem.wosWOS:000423291800030
hcfmusp.publisher.cityBASEL
hcfmusp.publisher.countrySWITZERLAND
hcfmusp.relation.referenceAbdel-Sayed S, 2003, AM J HYPERTENS, V16, P515, DOI 10.1016/S0895-7061(03)00903-8
hcfmusp.relation.referenceAhmed R, 2017, EVID-BASED COMPL ALT, DOI 10.1155/2017/5370545
hcfmusp.relation.referenceALHENCGELAS F, 1989, J HYPERTENS, V7, pS9, DOI 10.1097/00004872-198909007-00003
hcfmusp.relation.referenceBenigni A, 2010, EMBO MOL MED, V2, P247, DOI 10.1002/emmm.201000080
hcfmusp.relation.referenceBidani AK, 2009, HYPERTENSION, V54, P393, DOI 10.1161/HYPERTENSIONAHA.109.133777
hcfmusp.relation.referenceBoivin V, 2001, KIDNEY INT, V59, P515, DOI 10.1046/j.1523-1755.2001.059002515.x
hcfmusp.relation.referenceBrembilla-Perrot B, 2005, EUROPACE, V7, P621, DOI 10.1016/j.eupc.2005.06.012
hcfmusp.relation.referenceChan JSD, 2000, MOL CELL BIOCHEM, V212, P73, DOI 10.1023/A:1007152821315
hcfmusp.relation.referenceCupples WA, 2007, AM J PHYSIOL-RENAL, V292, pF1105, DOI 10.1152/ajprenal.00194.2006
hcfmusp.relation.referenceDalal S, 2012, MOL CELL BIOCHEM, V364, P59, DOI 10.1007/s11010-011-1205-7
hcfmusp.relation.referenceDavel APC, 2008, AM J PHYSIOL-HEART C, V295, pH211, DOI 10.1152/ajpheart.00581.2007
hcfmusp.relation.referenceDeng J, 2004, MOL CELL BIOL, V24, P10161, DOI 10.1128/MCB.24.23.10161-10168.2004
hcfmusp.relation.referenceDiBona GF, 1997, PHYSIOL REV, V77, P75
hcfmusp.relation.referenceDobrovolskaia MA, 2005, CURR CANCER DRUG TAR, V5, P325, DOI 10.2174/1568009054629645
hcfmusp.relation.referenceEMORI T, 1991, HYPERTENSION, V18, P165, DOI 10.1161/01.HYP.18.2.165
hcfmusp.relation.referenceFu YC, 2004, CARDIOVASC RES, V62, P558, DOI 10.1016/j.cardiores.2004.01.039
hcfmusp.relation.referenceGuijarro C, 2001, KIDNEY INT, V59, P415, DOI 10.1046/j.1523-1755.2001.059002415.x
hcfmusp.relation.referenceJohns EJ, 2011, COMPR PHYSIOL, V1, P731, DOI 10.1002/cphy.c100043
hcfmusp.relation.referenceKao MPC, 2010, J HUM HYPERTENS, V24, P1, DOI 10.1038/jhh.2009.70
hcfmusp.relation.referenceKobori H, 2001, J AM SOC NEPHROL, V12, P431
hcfmusp.relation.referenceKON V, 1989, MINER ELECTROL METAB, V15, P33
hcfmusp.relation.referenceCasare FAM, 2016, AM J PHYSIOL-RENAL, V310, pF1295, DOI 10.1152/ajprenal.00471.2015
hcfmusp.relation.referenceMalpas SC, 2010, PHYSIOL REV, V90, P513, DOI 10.1152/physrev.00007.2009
hcfmusp.relation.referenceMohamed SS, 2015, BIOCHEM PHARMACOL, V98, P403, DOI 10.1016/j.bcp.2015.10.004
hcfmusp.relation.referenceMoniri NH, 2007, BIOCHEM PHARMACOL, V74, P64, DOI 10.1016/j.bcp.2007.01.016
hcfmusp.relation.referenceNavar LG, 2001, J RENIN-ANGIO-ALDO S, V2, pS176, DOI 10.1177/14703203010020013001
hcfmusp.relation.referenceNirmala C, 1996, MOL CELL BIOCHEM, V159, P85, DOI 10.1007/BF00420910
hcfmusp.relation.referenceOliveira-Souza M, 2002, KIDNEY INT, V62, P1693, DOI 10.1046/j.1523-1755.2002.00604.x
hcfmusp.relation.referenceOLTVAI ZN, 1993, CELL, V74, P609, DOI 10.1016/0092-8674(93)90509-O
hcfmusp.relation.referenceRuster C, 2006, J AM SOC NEPHROL, V17, P2985, DOI 10.1681/ASN.2006040356
hcfmusp.relation.referenceSchlaich MP, 2009, J AM SOC NEPHROL, V20, P933, DOI 10.1681/ASN.2008040402
hcfmusp.relation.referenceSchonthal A.H., 2012, SCIENTIFICA, DOI 10.6064/2012/857516)
hcfmusp.relation.referenceShimizu MHM, 2013, EXP GERONTOL, V48, P298, DOI 10.1016/j.exger.2012.11.006
hcfmusp.relation.referenceSIBONY M, 1993, HYPERTENSION, V21, P827, DOI 10.1161/01.HYP.21.6.827
hcfmusp.relation.referenceTaniguchi M, 2015, CURR OPIN NEPHROL HY, V24, P345, DOI 10.1097/MNH.0000000000000141
hcfmusp.relation.referenceThieme K, 2015, PLOS ONE, V10, DOI 10.1371/journal.pone.0122265
hcfmusp.relation.referenceWang TT, 1998, KIDNEY INT, V54, P785, DOI 10.1046/j.1523-1755.1998.00069.x
hcfmusp.relation.referenceYokoyama T, 1997, CIRCULATION, V95, P1247
hcfmusp.relation.referenceZoccali C, 2002, CIRCULATION, V105, P1354, DOI 10.1161/hc1102.105261
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