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dc.contributor.author Orlowski, Alejandro
dc.contributor.author Ciancio, Maria Carolina
dc.contributor.author Caldiz, Claudia Irma
dc.contributor.author de Giusti, Verónica Celeste
dc.contributor.author Aiello, Ernesto Alejandro
dc.date.available 2018-01-16T18:28:32Z
dc.date.issued 2014-02
dc.identifier.citation Ciancio, Maria Carolina; Caldiz, Claudia Irma; Aiello, Ernesto Alejandro; de Giusti, Verónica Celeste; Orlowski, Alejandro; Reduced sarcolemmal expression and function of the NBCe1 isoform of the Na+–HCO3− cotransporter in hypertrophied cardiomyocytes of spontaneously hypertensive rats: role of the renin–angiotensin system; Oxford University Press; Cardiovascular Research; 101; 2; 2-2014; 211-219
dc.identifier.issn 0008-6363
dc.identifier.uri http://hdl.handle.net/11336/33457
dc.description.abstract Aims Electroneutral (NBCn1) and electrogenic (NBCe1) isoforms of the Na+–HCO3− cotransporter (NBC) coexist in the heart. We studied the expression and function of these isoforms in hearts of Wistar and spontaneously hypertensive rats (SHR), elucidating the direct implication of the renin–angiotensin system in the NBC regulation. Methods and results We used myocytes from Wistar, SHR, losartan-treated SHR (Los-SHR), and Angiotensin II (Ang II)-induced cardiac hypertrophy. We found an overexpression of NBCe1 and NBCn1 proteins in SHR that was prevented in Los-SHR. Hyperkalaemic-induced pHi alkalization was used to study selective activation of NBCe1. Despite the increase in NBCe1 expression, its activity was lower in SHR than in Wistar or Los-SHR. Similar results were found in Ang II-induced hypertrophy. A specific inhibitory antibody against NBCe1 allowed the discrimination between NBCe1 and NBCn1 activity. Whereas in SHR most of the pHi recovery was due to NBCn1 stimulation, in Wistar and Los-SHR the activity of both isoforms was equitable, suggesting that the deteriorated cardiac NBCe1 function observed in SHR is compensated by an enhanced activity of NBCn1. Using the biotin method, we observed greater level of internalized NBCe1 protein in SHR than in the non-hypertophic groups, while with immunofluorescence we localized the protein in endosomes near the nucleus only in SHR. Conclusions We conclude that Ang II is responsible for the impairment of the NBCe1 in hypertrophied hearts. This is due to retained transporter protein units in early endosomes. Moreover, NBCn1 activity seems to be increased in the hypertrophic myocardium of SHR, compensating impaired function of NBCe1.
dc.format application/pdf
dc.language.iso eng
dc.publisher Oxford University Press
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject Na+–HCO3 cotransporter
dc.subject Cardiac myocytes
dc.subject Cardiac hypertrophy
dc.subject.classification Inmunología
dc.subject.classification Medicina Básica
dc.subject.classification CIENCIAS MÉDICAS Y DE LA SALUD
dc.title Reduced sarcolemmal expression and function of the NBCe1 isoform of the Na+–HCO3− cotransporter in hypertrophied cardiomyocytes of spontaneously hypertensive rats: role of the renin–angiotensin system
dc.type info:eu-repo/semantics/article
dc.type info:ar-repo/semantics/artículo
dc.type info:eu-repo/semantics/publishedVersion
dc.date.updated 2018-01-03T19:16:36Z
dc.journal.volume 101
dc.journal.number 2
dc.journal.pagination 211-219
dc.journal.pais Reino Unido
dc.journal.ciudad Oxford
dc.description.fil Fil: Orlowski, Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
dc.description.fil Fil: Ciancio, Maria Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
dc.description.fil Fil: Caldiz, Claudia Irma. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
dc.description.fil Fil: de Giusti, Verónica Celeste. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
dc.description.fil Fil: Aiello, Ernesto Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
dc.journal.title Cardiovascular Research
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/cardiovascres/article/101/2/211/324814
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1093/cvr/cvt255
dc.conicet.fuente unificacion


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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)