Mineralocorticoids modulate the expression of the b-3 subunit of the Na+, K+ - ATPase in the renal collecting duct
Author
dc.contributor.author
Rojas, Macarena
Author
dc.contributor.author
Díaz Moreno, Pablo
Author
dc.contributor.author
León, Pablo
Author
dc.contributor.author
González, Alexis A.
Author
dc.contributor.author
González, Magdalena
Author
dc.contributor.author
Barrientos, Víctor
Author
dc.contributor.author
Pestov, Nikolay B.
Author
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Alzamora Miranda, Rodrigo
Author
dc.contributor.author
Michea Acevedo, Luis
Admission date
dc.date.accessioned
2018-06-13T19:47:30Z
Available date
dc.date.available
2018-06-13T19:47:30Z
Publication date
dc.date.issued
2017
Cita de ítem
dc.identifier.citation
Channels, 2017, Vol. 11, No. 5, 388–398
es_ES
Identifier
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10.1080/19336950.2017.1344800
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/148839
Abstract
dc.description.abstract
Renal sodium reabsorption depends on the activity of the Na+,K+-ATPase / heterodimer. Four ((1-4)) and 3 ((1-3)) subunit isoforms have been described. It is accepted that renal tubule cells express (1)/(1) dimers. Aldosterone stimulates Na+,K+-ATPase activity and may modulate (1)/(1) expression. However, some studies suggest the presence of (3) in the kidney. We hypothesized that the (3) isoform of the Na+,K+-ATPase is expressed in tubular cells of the distal nephron, and modulated by mineralocorticoids. We found that (3) is highly expressed in collecting duct of rodents, and that mineralocorticoids decreased the expression of (3). Thus, we describe a novel molecular mechanism of sodium pump modulation that may contribute to the effects of mineralocorticoids on sodium reabsorption.
es_ES
Patrocinador
dc.description.sponsorship
FONDECYT-Regular
1130550
1151423
FONDECYT-Iniciacion
11121217
CONICYT-Doctorado
21120658
Millennium Institute on Immunology and Immunotherapy (MIII)
P09/016-F
Millennium Nucleus of Ion Channels-Associated Diseases
MiNICAD NC160011