WNK4 limits distal calcium losses following acute furosemide treatment.
Animals
Calcium Channels
/ genetics
Calcium, Dietary
/ metabolism
Diuretics
/ toxicity
Furosemide
/ toxicity
Kidney Tubules, Proximal
/ drug effects
Male
Mice
Mice, Inbred C57BL
Protein Serine-Threonine Kinases
/ genetics
Renal Elimination
Renal Insufficiency
/ etiology
Sodium
/ metabolism
TRPV Cation Channels
/ genetics
Calcium
WNK4
distal convoluted tubule
thick ascending limb
Journal
Physiological reports
ISSN: 2051-817X
Titre abrégé: Physiol Rep
Pays: United States
ID NLM: 101607800
Informations de publication
Date de publication:
09 2019
09 2019
Historique:
received:
23
05
2019
revised:
26
06
2019
accepted:
27
06
2019
entrez:
10
9
2019
pubmed:
10
9
2019
medline:
19
8
2020
Statut:
ppublish
Résumé
The distal nephron is essential for calcium homeostasis. This is evidenced by disordered calcium transport following disrupted distal nephron function occurring in salt-wasting tubulopathies or with diuretic use. A plethora of studies support a role for WNK4 in thick ascending limb (TAL) and distal convoluted tubule ion transport with most studies focusing on sodium transport. Little is known about the in vivo role of WNK4 in regulating calcium homeostsis. Here, we investigated the role of WNK4 in regulating distal nephron calcium transport using WNK4 knockout animals (WNK4
Identifiants
pubmed: 31496133
doi: 10.14814/phy2.14195
pmc: PMC6732491
doi:
Substances chimiques
Calcium Channels
0
Calcium, Dietary
0
Diuretics
0
TRPV Cation Channels
0
Trpv5 protein, mouse
0
Furosemide
7LXU5N7ZO5
Sodium
9NEZ333N27
Prkwnk4 protein, mouse
EC 2.7.1.-
Protein Serine-Threonine Kinases
EC 2.7.11.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e14195Subventions
Organisme : American Heart Association-American Stroke Association
ID : 17POST33670206
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK051496
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK098141
Pays : United States
Organisme : NIDDK NIH HHS
ID : T32 DK007569
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.
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