Rapid Aldosterone-Mediated Signaling in the DCT Increases Activity of the Thiazide-Sensitive NaCl Cotransporter.
Aldosterone
/ metabolism
Animals
Blood Pressure
Calcium
/ metabolism
Cell Line
Cell Membrane
/ metabolism
Computational Biology
Cyclic AMP
/ metabolism
ErbB Receptors
/ metabolism
Gitelman Syndrome
/ metabolism
Kidney
/ metabolism
Kidney Tubules, Distal
/ metabolism
Male
Mice
Mineralocorticoids
/ metabolism
Phosphorylation
Proteomics
Receptors, Estrogen
/ metabolism
Receptors, G-Protein-Coupled
/ metabolism
Signal Transduction
Sodium Chloride
/ metabolism
Solute Carrier Family 12, Member 3
/ metabolism
Thiazides
/ pharmacology
Na transport
SPAK
cotransporter
epidermal growth factor receptor
mineralocorticoid
systems biology
Journal
Journal of the American Society of Nephrology : JASN
ISSN: 1533-3450
Titre abrégé: J Am Soc Nephrol
Pays: United States
ID NLM: 9013836
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
received:
17
10
2018
accepted:
29
04
2019
pubmed:
30
6
2019
medline:
28
4
2020
entrez:
30
6
2019
Statut:
ppublish
Résumé
The NaCl cotransporter NCC in the kidney distal convoluted tubule (DCT) regulates urinary NaCl excretion and BP. Aldosterone increases NaCl reabsorption Proteomics, bioinformatics, and cell biology approaches were combined with animal models and gene-targeted mice. Aldosterone significantly increases NCC activity within minutes Aldosterone acutely activates NCC to modulate renal NaCl excretion.
Sections du résumé
BACKGROUND
The NaCl cotransporter NCC in the kidney distal convoluted tubule (DCT) regulates urinary NaCl excretion and BP. Aldosterone increases NaCl reabsorption
METHODS
Proteomics, bioinformatics, and cell biology approaches were combined with animal models and gene-targeted mice.
RESULTS
Aldosterone significantly increases NCC activity within minutes
CONCLUSIONS
Aldosterone acutely activates NCC to modulate renal NaCl excretion.
Identifiants
pubmed: 31253651
pii: ASN.2018101025
doi: 10.1681/ASN.2018101025
pmc: PMC6683706
doi:
Substances chimiques
GPER1 protein, mouse
0
Mineralocorticoids
0
Receptors, Estrogen
0
Receptors, G-Protein-Coupled
0
Slc12a3 protein, mouse
0
Solute Carrier Family 12, Member 3
0
Thiazides
0
Sodium Chloride
451W47IQ8X
Aldosterone
4964P6T9RB
Cyclic AMP
E0399OZS9N
ErbB Receptors
EC 2.7.10.1
Calcium
SY7Q814VUP
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1454-1470Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK110621
Pays : United States
Informations de copyright
Copyright © 2019 by the American Society of Nephrology.
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