| Literature DB >> 28636485 |
Macarena Rojas1, Pablo Díaz1, Pablo León1, Alexis A Gonzalez2, Magdalena González1, Víctor Barrientos1, Nikolay B Pestov3,4, Rodrigo Alzamora1,5, Luis Michea1,6.
Abstract
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.Entities:
Keywords: aldosterone; epithelial sodium channel; hypertension; intercalated cells; pendrin; principal cells; sodium pump
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Year: 2017 PMID: 28636485 PMCID: PMC5626372 DOI: 10.1080/19336950.2017.1344800
Source DB: PubMed Journal: Channels (Austin) ISSN: 1933-6950 Impact factor: 2.581