Role of inwardly rectifying K+ channel 5.1 (Kir5.1) in the regulation of renal membrane transport.
Journal
Current opinion in nephrology and hypertension
ISSN: 1473-6543
Titre abrégé: Curr Opin Nephrol Hypertens
Pays: England
ID NLM: 9303753
Informations de publication
Date de publication:
01 09 2022
01 09 2022
Historique:
aheadofprint:
12
07
2022
entrez:
27
7
2022
pubmed:
28
7
2022
medline:
29
7
2022
Statut:
ppublish
Résumé
Kir5.1 interacts with Kir4.2 in proximal tubule and with Kir4.1 in distal convoluted tubule (DCT), connecting tubule (CNT) and cortical collecting duct (CCD) to form basolateral-K+-channels. Kir4.2/Kir5.1 and Kir4.1/Kir5.1 play an important role in regulating Na+/HCO3--transport of the proximal tubule and Na+/K+ -transport in the DCT/CNT/CCD. The main focus of this review is to provide an overview of the recent development in the field regarding the role of Kir5.1 regulating renal electrolyte transport in the proximal tubule and DCT. Loss-of-function-mutations of KCNJ16 cause a new form of tubulopathy, characterized by hypokalaemia, Na+-wasting, acid-base-imbalance and metabolic-acidosis. Abnormal bicarbonate transport induced by loss-of-function of KCNJ16-mutants is recapitulated in Kir4.2-knockout-(Kir4.2 KO) mice. Deletion of Kir5.1 also abolishes the effect of dietary Na+ and K+-intakes on the basolateral membrane voltage and NCC expression/activity. Long-term high-salt intake or high-K+-intake causes hyperkalaemic in Kir5.1-deficient mice. Kir4.2/Kir5.1 activity in the proximal tubule plays a key role in regulating Na+, K+ and bicarbonate-transport through regulating electrogenic-Na+-bicarbonate-cotransporter-(NBCe1) and type 3-Na+/H+-exchanger-(NHE3). Kir4.1/Kir5.1 activity of the DCT plays a critical role in mediating the effect of dietary-K+ and Na+-intakes on NCC activity/expression. As NCC determines the Na+ delivery rate to the aldosterone-sensitive distal nephron (ASDN), defective regulation of NCC during high-salt and high-K+ compromises renal K+ excretion and K+ homeostasis.
Identifiants
pubmed: 35894283
doi: 10.1097/MNH.0000000000000817
pii: 00041552-202209000-00013
doi:
Substances chimiques
Bicarbonates
0
Potassium Channels, Inwardly Rectifying
0
Sodium
9NEZ333N27
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
479-485Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK115366
Pays : United States
Organisme : NIDDK NIH HHS
ID : R56 DK054983
Pays : United States
Informations de copyright
Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.
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