Does the early aldosterone‐induced SGK1 play a role in early Kaliuresis?
Author:
Affiliation:
1. Division of Nephrology Johns Hopkins University School of Medicine Baltimore USA
2. Department of Biomedical Sciences University of Lausanne Lausanne Switzerland
3. Department of Physiology University of Maryland Baltimore USA
Publisher
Wiley
Subject
Physiology (medical),Physiology
Link
https://onlinelibrary.wiley.com/doi/pdf/10.14814/phy2.15188
Reference51 articles.
1. Defective regulation of the epithelial Na+ channel by Nedd4 in Liddle's syndrome
2. Renal Tubular Ubiquitin-Protein Ligase NEDD4-2 Is Required for Renal Adaptation during Long-Term Potassium Depletion
3. Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC
4. The Serum and Glucocorticoid Kinase sgk Increases the Abundance of Epithelial Sodium Channels in the Plasma Membrane of Xenopus Oocytes
5. Nedd4-2 Modulates Renal Na+-Cl−Cotransporter via the Aldosterone-SGK1-Nedd4-2 Pathway
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1. Klotho is highly expressed in the chief sites of regulated potassium secretion, and it is stimulated by potassium intake;Scientific Reports;2024-05-10
2. Renal tubular SGK1 is required to achieve blood pressure surge and circadian rhythm;American Journal of Physiology-Renal Physiology;2023-11-01
3. Dietary anions control potassium excretion: it is more than a poorly absorbable anion effect;American Journal of Physiology-Renal Physiology;2023-09-01
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