ArticleJournal of the American Society of Nephrology : JASN2015
Mechanisms of renal control of potassium homeostasis in complete aldosterone deficiency.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 81 citations in OpenAlex.
- The kidney distal tubule potassium switch, modern diet and hypertension.Nature reviews. Nephrology · 2026Review
- Potassium and the kidney.Nature reviews. Nephrology · 2026Review
- Sex differences in potassium regulation: evidence, molecular mechanisms and clinical implications.Biology of sex differences · 2026Review
- The exquisite link between potassium homeostasis regulation and cardiovascular health: exploration and analysis.Frontiers in physiology · 2026Review
- Aldosterone-identified targets for optimal sodium and potassium supplementation in intestinal failure.Frontiers in nutrition · 2026Article
- Canagliflozin Inhibits Electrogenic Na+ Transport in Mouse Cortical Collecting Duct Cells.Function (Oxford, England) · 2025Article
- Electrophysiology Models for End-Stage Renal Disease Maladaptations That Promote Asystole.Reviews in cardiovascular medicine · 2025Review
- Impact of aldosterone deficiency on the development of diuretic resistance in mice.Pflugers Archiv : European journal of physiology · 2025Article
- Aldosterone-independent regulation of K + secretion in the distal nephron.Current opinion in nephrology and hypertension · 2024Review
- Klotho is highly expressed in the chief sites of regulated potassium secretion, and it is stimulated by potassium intake.Scientific reports · 2024Article
- Extra-adrenal aldosterone: a mini review focusing on the physiology and pathophysiology of intrarenal aldosterone.Endocrine · 2024Review
- Dietary anions control potassium excretion: it is more than a poorly absorbable anion effect.American journal of physiology. Renal physiology · 2023Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Pendrin regulation is prioritized by anion in high-potassium diets.American journal of physiology. Renal physiology · 2023Article
- Collecting duct renin regulates potassium homeostasis in mice.Acta physiologica (Oxford, England) · 2023Article
- Blood pressure effects of sodium transport along the distal nephron.Kidney international · 2022Review
- Regulation of distal tubule sodium transport: mechanisms and roles in homeostasis and pathophysiology.Pflugers Archiv : European journal of physiology · 2022Review
- Mineralocorticoid Receptor Antagonists Cause Natriuresis in the Absence of Aldosterone.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Tubular IL-1β Induces Salt Sensitivity in Diabetes by Activating Renal Macrophages.Circulation research · 2022Article
- Kidney-Specific CAP1/Prss8-Deficient Mice Maintain ENaC-Mediated Sodium Balance through an Aldosterone Independent Pathway.International journal of molecular sciences · 2022Article
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aldosterone-independent mechanisms may contribute to K(+) homeostasis. We studied aldosterone synthase knockout (AS(-/-)) mice to define renal control mechanisms of K(+) homeostasis in complete aldosterone deficiency. AS(-/-) mice were normokalemic and tolerated a physiologic dietary K(+) load (2% K(+), 2 days) without signs of illness, except some degree of polyuria. With supraphysiologic K(+) intake (5% K(+)), AS(-/-) mice decompensated and became hyperkalemic. High-K(+) diets induced upregulation of the renal outer medullary K(+) channel in AS(-/-) mice, whereas upregulation of the epithelial sodium channel (ENaC) sufficient to increase the electrochemical driving force for K(+) excretion was detected only with a 2% K(+) diet. Phosphorylation of the thiazide-sensitive NaCl cotransporter was consistently lower in AS(-/-) mice than in AS(+/+) mice and was downregulated in mice of both genotypes in response to increased K(+) intake. Inhibition of the angiotensin II type 1 receptor reduced renal creatinine clearance and apical ENaC localization, and caused severe hyperkalemia in AS(-/-) mice. In contrast with the kidney, the distal colon of AS(-/-) mice did not respond to dietary K(+) loading, as indicated by Ussing-type chamber experiments. Thus, renal adaptation to a physiologic, but not supraphysiologic, K(+) load can be achieved in aldosterone deficiency by aldosterone-independent activation of the renal outer medullary K(+) channel and ENaC, to which angiotensin II may contribute. Enhanced urinary flow and reduced activity of the thiazide-sensitive NaCl cotransporter may support renal adaptation by activation of flow-dependent K(+) secretion and increased intratubular availability of Na(+) that can be reabsorbed in exchange for K(+) secreted.
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