dc.creatorRojas, Macarena
dc.creatorDíaz, Pablo
dc.creatorLeón, Pablo
dc.creatorGonzález, Alexis A.
dc.creatorGonzález, Magdalena
dc.creatorBarrientos, Víctor
dc.creatorPestov, Nikolay B.
dc.creatorAlzamora, Rodrigo
dc.creatorMichea Acevedo, Luis
dc.date.accessioned2019-03-18T11:59:38Z
dc.date.available2019-03-18T11:59:38Z
dc.date.created2019-03-18T11:59:38Z
dc.date.issued2017
dc.identifierChannels, Volumen 11, Issue 5, 2018, Pages 388-398
dc.identifier19336969
dc.identifier19336950
dc.identifier10.1080/19336950.2017.1344800
dc.identifierhttps://repositorio.uchile.cl/handle/2250/167216
dc.description.abstract© 2017 Taylor & Francis. Renal sodium reabsorption depends on the activity of the Na+,K+-ATPase α/β heterodimer. Four α (α1–4) and 3 β (β1–3) subunit isoforms have been described. It is accepted that renal tubule cells express α1/β1 dimers. Aldosterone stimulates Na+,K+-ATPase activity and may modulate α1/β1 expression. However, some studies suggest the presence of β3 in the kidney. We hypothesized that the β3 isoform of the Na+,K+-ATPase is expressed in tubular cells of the distal nephron, and modulated by mineralocorticoids. We found that β3 is highly expressed in collecting duct of rodents, and that mineralocorticoids decreased the expression of β3. Thus, we describe a novel molecular mechanism of sodium pump modulation that may contribute to the effects of mineralocorticoids on sodium reabsorption.
dc.languageen
dc.publisherTaylor and Francis Inc.
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourceChannels
dc.subjectaldosterone
dc.subjectepithelial sodium channel
dc.subjecthypertension
dc.subjectintercalated cells
dc.subjectpendrin
dc.subjectprincipal cells
dc.subjectsodium pump
dc.titleMineralocorticoids modulate the expression of the β-3 subunit of the Na+, K+-ATPase in the renal collecting duct
dc.typeArtículo de revista


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