ArticleThe Journal of physiology2014
Functional coupling of renal K+ and Na+ handling causes high blood pressure in Na+ replete mice.
Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
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Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- Potassium Intake and Blood Pressure: A Dose-Response Meta-Analysis of Randomized Controlled Trials.Journal of the American Heart Association · 2020Pooled it
- Why Your Mother Was Right: How Potassium Intake Reduces Blood Pressure.Transactions of the American Clinical and Climatological Association · 2015Trial
- The kidney distal tubule potassium switch, modern diet and hypertension.Nature reviews. Nephrology · 2026Review
- Potassium and the kidney.Nature reviews. Nephrology · 2026Review
- How Does Dietary Potassium Influence BP?Journal of the American Society of Nephrology : JASN · 2026Review
- The endocytic adaptor ARH facilitates potassium conservation by regulating ROMK and BK.American journal of physiology. Renal physiology · 2025Article
- Combination of genetic studies and animal modeling proposes TMPRSS9 as a candidate gene for serum KScientific reports · 2025Article
- Potassium supplementation and depletion during development of salt-sensitive hypertension in male and female SS rats.JCI insight · 2025Article
- High chloride induces aldosterone resistance in the distal nephron.Acta physiologica (Oxford, England) · 2025Article
- Macrophage SPAK deletion limits a low potassium-induced kidney inflammatory program.American journal of physiology. Renal physiology · 2024Article
- Navigating the multifaceted intricacies of the NaPhysiological reviews · 2024Review
- Low potassium activation of proximal mTOR/AKT signaling is mediated by Kir4.2.Nature communications · 2024Article
- Potassium-Switch Signaling Pathway Dictates Acute Blood Pressure Response to Dietary Potassium.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Chronic kidney disease increases the susceptibility to negative effects of low and high potassium intake.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024Article
- Review Article on Molecular Mechanism of Regulation of Hypertension by Macro-elements (Na, K, Ca and Mg), Micro-elements/Trace Metals (Zn and Cu) and Toxic Elements (Pb and As).Biological trace element research · 2024Review
- Dietary sodium alters aldosterone's effect on renal sodium transporter expression and distal convoluted tubule remodelling.The Journal of physiology · 2024Article
- Modifying Dietary Sodium and Potassium Intake: An End to the 'Salt Wars'?Hypertension (Dallas, Tex. : 1979) · 2024Review
- Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure.The Journal of clinical investigation · 2023Article
- Male kidney-specific BMAL1 knockout mice are protected from KAmerican journal of physiology. Renal physiology · 2023Article
- The AE4 transporter mediates kidney acid-base sensing.Nature communications · 2023Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A network of kinases, including WNKs, SPAK and Sgk1, is critical for the independent regulation of K+ and Na+ transport in the distal nephron. Angiotensin II is thought to act as a key hormone in orchestrating these kinases to switch from K+ secretion during hyperkalaemia to Na+ reabsorption during intravascular volume depletion, thus keeping disturbances in electrolyte and blood pressure homeostasis at a minimum. It remains unclear, however, how K+ and Na+ transport are regulated during a high Na+ intake, which is associated with suppressed angiotensin II levels and a high distal tubular Na+ load. We therefore investigated the integrated blood pressure, renal, hormonal and gene and protein expression responses to large changes of K+ intake in Na+ replete mice. Both low and high K+ intake increased blood pressure and caused Na+ retention. Low K+ intake was accompanied by an upregulation of the sodium-chloride cotransporter (NCC) and its activating kinase SPAK, and inhibition of NCC normalized blood pressure. Renal responses were unaffected by angiotensin AT1 receptor antagonism, indicating that low K+ intake activates the distal nephron by an angiotensin-independent mode of action. High K+ intake was associated with elevated plasma aldosterone concentrations and an upregulation of the epithelial sodium channel (ENaC) and its activating kinase Sgk1. Surprisingly, high K+ intake increased blood pressure even during ENaC or mineralocorticoid receptor antagonism, suggesting the contribution of aldosterone-independent mechanisms. These findings show that in a Na+ replete state, changes in K+ intake induce specific molecular and functional adaptations in the distal nephron that cause a functional coupling of renal K+ and Na+ handling, resulting in Na+ retention and high blood pressure when K+ intake is either restricted or excessively increased.
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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.