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Severe hyperkalemia is rescued by low-potassium diet in renal beta ENaC-deficient mice

dc.contributor.authorBOSCARDIN, E.
dc.contributor.authorPERRIER, R.
dc.contributor.authorSERGI, C.
dc.contributor.authorMAILLARD, M.
dc.contributor.authorLOFFING, J.
dc.contributor.authorLOFFING-CUENI, D.
dc.contributor.authorKOESTERS, R.
dc.contributor.authorROSSIER, B. C.
dc.contributor.authorHUMMLER, E.
dc.date.accessioned2020-07-09T14:17:10Z
dc.date.available2020-07-09T14:17:10Z
dc.date.issued2017-10
dc.identifier.issn0031-6768
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/10353
dc.description.abstractEnIn adulthood, an induced nephron-specific deficiency of alpha ENaC (Scnn1a) resulted in pseudohypoaldosteronism type 1 (PHA-1) with sodium loss, hyperkalemia, and metabolic acidosis that is rescued through high-sodium/low-potassium (HNa+/LK+) diet. In the present study, we addressed whether renal beta ENaC expression is required for sodium and potassium balance or can be compensated by remaining (alpha and gamma) ENaC subunits using adult nephron-specific knockout (Scnn1b(Pax8/LC1)) mice. Upon induction, these mice present a severe PHA-1 phenotype with weight loss, hyperkalemia, and dehydration, but unlike the Scnn1a(Pax8/LC1) mice without persistent salt wasting. This is followed by a marked downregulation of STE20/SPS1-related proline-alanine-rich protein kinase (SPAK) and Na+/Cl- co-transporter (NCC) protein expression and activity. Most of the experimental Scnn1b(Pax8/LC1) mice survived with a HNa+/LK+ diet that partly normalized NCC phosphorylation, but not total NCC expression. Since salt loss was minor, we applied a standard-sodium/LK+ diet that efficiently rescued these mice resulting in normokalemia and normalization of NCC phosphorylation, but not total NCC expression. A further switch to LNa+/standard-K+ diet induced again a severe PHA-1-like phenotype, but with only transient salt wasting indicating that low-K+ intake is critical to decrease hyperkalemia in a NCC-dependent manner. In conclusion, while the beta ENaC subunit plays only a minor role in sodium balance, severe hyperkalemia results in downregulation of NCC expression and activity. Our data demonstrate the importance to primarily correct the hyperkalemia with a low-potassium diet that normalizes NCC activity.
dc.title.enSevere hyperkalemia is rescued by low-potassium diet in renal beta ENaC-deficient mice
dc.typeArticle de revue
dc.identifier.doi10.1007/s00424-017-1990-2
dc.subject.halChimie/Matériaux
bordeaux.journalPflugers Archiv-European Journal of Physiology
bordeaux.page1387-1399
bordeaux.volume469
bordeaux.hal.laboratoriesInstitut de Chimie & de Biologie des Membranes & des Nano-objets (CBMN) - UMR 5248*
bordeaux.hal.laboratoriesInstitut de Chimie & de Biologie des Membranes & des Nano-objets (CBMN, UMR 5248)
bordeaux.issue10
bordeaux.institutionUniversité de Bordeaux
bordeaux.institutionBordeaux INP
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