Increased NHE3 abundance and transport activity in renal proximal tubule of rats with heart failure

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dc.contributor Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP INOUE, Bruna H. FMUSP-HC
SANTOS, Leonardo dos
PESSOA, Thaissa D.
SAVIGNANO, Fernanda A.
TUCCI, Paulo J. F.
MALNIC, Gerhard
GIRARDI, Adriana C. C. FMUSP-HC 2012
dc.identifier.issn 0363-6119
dc.description.abstract Inoue BH, dos Santos L, Pessoa TD, Antonio EL, Pacheco BPM, Savignano FA, Carraro-Lacroix LR, Tucci PJF, Malnic G, Girardi ACC. Increased NHE3 abundance and transport activity in renal proximal tubule of rats with heart failure. Am J Physiol Regul Integr Comp Physiol 302: R166-R174, 2012. First published October 26, 2011; doi:10.1152/ajpregu.00127.2011.-Heart failure (HF) is associated with a reduced effective circulating volume that drives sodium and water retention and extracellular volume expansion. We therefore hypothesized that Na(+)/H(+) exchanger isoform 3 (NHE3), the major apical transcellular pathway for sodium reabsorption in the proximal tubule, is upregulated in an experimental model of HF. HF was induced in male rats by left ventricle radiofrequency ablation. Sham-operated rats (sham) were used as controls. At 6 wk after surgery, HF rats exhibited cardiac dysfunction with a dramatic increase in left ventricular end-diastolic pressure. By means of stationary in vivo microperfusion and pH-dependent sodium uptake, we demonstrated that NHE3 transport activity was significantly higher in the proximal tubule of HF compared with sham rats. Increased NHE3 activity was paralleled by increased renal cortical NHE3 expression at both protein and mRNA levels. In addition, the baseline PKA-dependent NHE3 phosphorylation at serine 552 was reduced in renal cortical membranes of rats with HF. Collectively, these results suggest that NHE3 is upregulated in the proximal tubule of HF rats by transcriptional, translational, and posttranslational mechanisms. Enhanced NHE3-mediated sodium reabsorption in the proximal tubule may contribute to extracellular volume expansion and edema, the hallmark feature of HF. Moreover, our study emphasizes the importance of undertaking a cardiorenal approach to contain progression of cardiac disease.
dc.description.sponsorship · Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
· Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
· Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
dc.language.iso eng
dc.relation.ispartof American Journal of Physiology-Regulatory Integrative and Comparative Physiology
dc.rights restrictedAccess
dc.subject myocardial injury; renal function; volume homeostasis; radiofrequency ablation
dc.subject.other atrial-natriuretic-peptide; na+/h+ exchanger nhe3; spontaneously hypertensive rat; angiotensin-aldosterone system; acute myocardial-infarction; thick ascending limb; unifying hypothesis; extracellular fluid; sodium retention; epithelial-cells
dc.title Increased NHE3 abundance and transport activity in renal proximal tubule of rats with heart failure
dc.type article
dc.rights.holder Copyright AMER PHYSIOLOGICAL SOC LIM/13
dc.identifier.doi 10.1152/ajpregu.00127.2011
dc.identifier.pmid 22031782
dc.type.category original article
dc.type.version publishedVersion INOUE, Bruna H.:FM: PACHECO, Bruna P. M.:FM: GIRARDI, Adriana C. C.:HC:INCOR · SANTOS, Leonardo dos:Univ Sao Paulo, Heart Inst InCor, Sch Med, BR-05403900 Sao Paulo, Brazil; Univ Fed Espirito Santo, Dept Physiol Sci, Vitoria, ES, Spain
· PESSOA, Thaissa D.:Univ Sao Paulo, Dept Physiol & Biophys, Inst Biomed Sci, BR-05403900 Sao Paulo, Brazil
· ANTONIO, Ednei L.:Univ Fed Sao Paulo, Dept Physiol, Sao Paulo, Brazil
· SAVIGNANO, Fernanda A.:Univ Sao Paulo, Heart Inst InCor, Sch Med, BR-05403900 Sao Paulo, Brazil
· CARRARO-LACROIX, Luciene R.:Univ Sao Paulo, Dept Physiol & Biophys, Inst Biomed Sci, BR-05403900 Sao Paulo, Brazil
· TUCCI, Paulo J. F.:Univ Fed Sao Paulo, Dept Physiol, Sao Paulo, Brazil
· MALNIC, Gerhard:Univ Sao Paulo, Dept Physiol & Biophys, Inst Biomed Sci, BR-05403900 Sao Paulo, Brazil WOS:000298666700019 2-s2.0-84255168958 BETHESDA USA
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dc.description.index MEDLINE
hcfmusp.citation.scopus 22
hcfmusp.citation.wos 20 Brasil Espanha

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