ArticlePloS one2015
Low Na, high K diet and the role of aldosterone in BK-mediated K excretion.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- The endocytic adaptor ARH facilitates potassium conservation by regulating ROMK and BK.American journal of physiology. Renal physiology · 2025Article
- Article
- GDF15, an Emerging Player in Renal Physiology and Pathophysiology.International journal of molecular sciences · 2024Review
- Review
- ER ribosomal-binding protein 1 regulates blood pressure and potassium homeostasis by modulating intracellular renin trafficking.Journal of biomedical science · 2023Article
- Renal KFrontiers in physiology · 2023Review
- Intercalated cell BKα subunit is required for flow-induced K+ secretion.JCI insight · 2020Article
- Stimulatory Role of SPAK Signaling in the Regulation of Large Conductance CaFrontiers in physiology · 2020Article
- Potassium-sparing effects of furosemide in mice on high-potassium diets.American journal of physiology. Renal physiology · 2019Review
- Furosemide reduces BK-αβ4-mediated KAmerican journal of physiology. Renal physiology · 2019Article
- Renal and colonic potassium transporters in the pregnant rat.American journal of physiology. Renal physiology · 2018Article
- Aldosterone, SGK1, and ion channels in the kidney.Clinical science (London, England : 1979) · 2018Review
- Net KKidney international · 2017Article
- The renal response to potassium stress: integrating past with present.Current opinion in nephrology and hypertension · 2017Review
- Renal Tubular Ubiquitin-Protein Ligase NEDD4-2 Is Required for Renal Adaptation during Long-Term Potassium Depletion.Journal of the American Society of Nephrology : JASN · 2017Article
- Molecular Mechanisms Underlying Renin-Angiotensin-Aldosterone System Mediated Regulation of BK Channels.Frontiers in physiology · 2017Review
- Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC.American journal of physiology. Renal physiology · 2016Article
- Maintaining KAmerican journal of physiology. Renal physiology · 2016Review
- Potassium and Its Discontents: New Insight, New Treatments.Journal of the American Society of Nephrology : JASN · 2016Review
- Cell-specific regulation of L-WNK1 by dietary K.American journal of physiology. Renal physiology · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
A low Na, high K diet (LNaHK) is associated with a low rate of cardiovascular (CV) disease in many societies. Part of the benefit of LNaHK relies on its diuretic effects; however, the role of aldosterone (aldo) in the diuresis is not understood. LNaHK mice exhibit an increase in renal K secretion that is dependent on the large, Ca-activated K channel, (BK-α with accessory BK-β4; BK-α/β4). We hypothesized that aldo causes an osmotic diuresis by increasing BK-α/β4-mediated K secretion in LNaHK mice. We found that the plasma aldo concentration (P[aldo]) was elevated by 10-fold in LNaHK mice compared with control diet (Con) mice. We subjected LNaHK mice to either sham surgery (sham), adrenalectomy (ADX) with low aldo replacement (ADX-LA), or ADX with high aldo replacement (ADX-HA). Compared to sham, the urinary flow, K excretion rate, transtubular K gradient (TTKG), and BK-α and BK-β4 expressions, were decreased in ADX-LA, but not different in ADX-HA. BK-β4 knockout (β4KO) and WT mice exhibited similar K clearance and TTKG in the ADX-LA groups; however, in sham and ADX-HA, the K clearance and TTKG of β4KO were less than WT. In response to amiloride treatment, the osmolar clearance was increased in WT Con, decreased in WT LNaHK, and unchanged in β4KO LNaHK. These data show that the high P[aldo] of LNaHK mice is necessary to generate a high rate of BK-α/β4-mediated K secretion, which creates an osmotic diuresis that may contribute to a reduction in CV disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.