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Channels (Austin). 2017 Sep 3;11(5):388-398. doi: 10.1080/19336950.2017.1344800. Epub 2017 Jun 21.

Mineralocorticoids modulate the expression of the β-3 subunit of the Na+, K+-ATPase in the renal collecting duct.

Author information

1
a Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile , Santiago , Chile.
2
b Instituto de Química, Pontificia Universidad Católica de Valparaíso , Valparaíso , Chile.
3
c Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry , Moscow , Russia.
4
d Department of Physiology and Pharmacology and Center for Diabetes and Endocrine Research , University of Toledo College of Medicine , Toledo , OH , USA.
5
e Millennium Nucleus of Ion Channels-Associated Diseases (MiNICAD) , Santiago , Chile.
6
f Millennium Institute on Immunology and Immunotherapy , Santiago , Chile.

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 α11 dimers. Aldosterone stimulates Na+,K+-ATPase activity and may modulate α11 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.

KEYWORDS:

aldosterone; epithelial sodium channel; hypertension; intercalated cells; pendrin; principal cells; sodium pump

PMID:
28636485
PMCID:
PMC5626372
DOI:
10.1080/19336950.2017.1344800
[Indexed for MEDLINE]
Free PMC Article

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