Regulation of Distal Nephron Transport by Intracellular Chloride and Potassium.
Malpighian tubule
Oxidative stress response 1
Sodium chloride cotransporter
Ste20-related proline-alanine-rich kinase
With No Lysine [K]
Journal
Nephron
ISSN: 2235-3186
Titre abrégé: Nephron
Pays: Switzerland
ID NLM: 0331777
Informations de publication
Date de publication:
2023
2023
Historique:
received:
23
04
2022
accepted:
11
07
2022
pmc-release:
01
01
2024
medline:
6
4
2023
pubmed:
18
8
2022
entrez:
17
8
2022
Statut:
ppublish
Résumé
Low potassium increases the phosphorylation and activity of the sodium chloride cotransporter (NCC) in the distal convoluted tubule of the nephron, which contributes to the hypertensive effect of the modern low potassium/high sodium diet. A central mediator of potassium regulation of NCC is the chloride-sensitive With No Lysine [K] (WNK) kinase. Chloride directly inhibits WNKs by binding to the active site. The mechanisms underlying WNK regulation by extracellular potassium are reviewed, as well as the modulatory effect of kidney-specific-WNK1. WNK1, but not WNK1 kinase activity, is also required for the aldosterone-independent regulation of the epithelial sodium channel by potassium. Whether intracellular chloride could be involved in this process is discussed. Recent studies demonstrating direct regulation of WNKs by intracellular potassium are also reviewed, and the potential physiological relevance to renal epithelial ion transport is discussed. WNKs are sensors of the intracellular ionic milieu. In the nephron, changes in extracellular ion concentrations, resulting in changes in intracellular ion concentration, regulate WNK activity and downstream transporters and channels to maintain total body ion homeostasis.
Sections du résumé
BACKGROUND
Low potassium increases the phosphorylation and activity of the sodium chloride cotransporter (NCC) in the distal convoluted tubule of the nephron, which contributes to the hypertensive effect of the modern low potassium/high sodium diet. A central mediator of potassium regulation of NCC is the chloride-sensitive With No Lysine [K] (WNK) kinase.
SUMMARY
Chloride directly inhibits WNKs by binding to the active site. The mechanisms underlying WNK regulation by extracellular potassium are reviewed, as well as the modulatory effect of kidney-specific-WNK1. WNK1, but not WNK1 kinase activity, is also required for the aldosterone-independent regulation of the epithelial sodium channel by potassium. Whether intracellular chloride could be involved in this process is discussed. Recent studies demonstrating direct regulation of WNKs by intracellular potassium are also reviewed, and the potential physiological relevance to renal epithelial ion transport is discussed.
KEY MESSAGES
WNKs are sensors of the intracellular ionic milieu. In the nephron, changes in extracellular ion concentrations, resulting in changes in intracellular ion concentration, regulate WNK activity and downstream transporters and channels to maintain total body ion homeostasis.
Identifiants
pubmed: 35977527
pii: 000526051
doi: 10.1159/000526051
pmc: PMC9935751
mid: NIHMS1824738
doi:
Substances chimiques
Protein Serine-Threonine Kinases
EC 2.7.11.1
Potassium
RWP5GA015D
Chlorides
0
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
203-211Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK110358
Pays : United States
Informations de copyright
© 2022 S. Karger AG, Basel.
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