Adriana Marton, Hieu T N Tran, Norihiko Morisawa, Ismail Osman, Seyed Ehsan Saffari, Tzy Tiing Lim, Wan Keat Yam, Matthew B Chuah, Wei Lin Tay, Wai Lun Moy, Pek-Lan Khong, Calvin W L Chin, Armin M Nagel, Roger S Y Foo, Friedrich C Luft, Eric Finkelstein, Jean-Paul Kovalik, Manfred Rauh, Troy Puar, Jens Titze
{"title":"Oral KCl Supplementation Safely Reduces Body Na<sup>+</sup> Surplus and Blood Pressure.","authors":"Adriana Marton, Hieu T N Tran, Norihiko Morisawa, Ismail Osman, Seyed Ehsan Saffari, Tzy Tiing Lim, Wan Keat Yam, Matthew B Chuah, Wei Lin Tay, Wai Lun Moy, Pek-Lan Khong, Calvin W L Chin, Armin M Nagel, Roger S Y Foo, Friedrich C Luft, Eric Finkelstein, Jean-Paul Kovalik, Manfred Rauh, Troy Puar, Jens Titze","doi":"10.1161/CIRCRESAHA.126.329131","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Potassium-enriched table salt lowers blood pressure (BP) and reduces cardiovascular mortality. Whether these beneficial effects stem from reduced Na<sup>+</sup> intake, increased K<sup>+</sup> intake, or both is unknown. We tested the hypothesis that oral potassium chloride (KCl) supplementation lowers body Na<sup>+</sup> content and BP in patients with essential hypertension (EH) or hyperaldosteronism, independent of salt intake.</p><p><strong>Methods: </strong>Between February 2024 and February 2025, we conducted a single-arm, prospective, longitudinal study with nonrandomized oral KCl intervention in 40 participants with hypertension. All received personalized (blood K<sup>+</sup>-adjusted) KCl supplementation (Span-K tablets) for 6 to 9 weeks. After the intervention, participants completed a routine diagnostic workup and were classified with EH or hyperaldosteronism. Primary end point: baseline muscle Na<sup>+</sup> surplus in hyperaldosteronism. Secondary end point: interventional muscle Na<sup>+</sup> mobilization and BP reduction.</p><p><strong>Results: </strong>Seventeen participants were diagnosed with EH, and 23 with hyperaldosteronism. At baseline, patients with hyperaldosteronism showed higher muscle Na<sup>+</sup> content (24.67±2.93 versus 22.48±3.37 mmol/L tissue volume, <i>P</i>=0.023; primary end point). Oral KCl increased 24-hour urine K<sup>+</sup> excretion without altering 24-hour urine Na<sup>+</sup>. KCl supplementation successfully eliminated the muscle Na<sup>+</sup> surplus in the hyperaldosteronism group (-1.90 mmol/L tissue volume [CI, -3.20 to -0.60]; <i>P</i>=0.005; secondary end point), lowered blood Na<sup>+</sup>/K<sup>+</sup> ratios in both groups (EH, -5.34 [CI, -7.69 to -2.99]; <i>P</i>=4.6×10<sup>-5</sup>; hyperaldosteronism, -7.02 [CI, -9.04 to -5.01]; <i>P</i>=2.1×10<sup>-8</sup>), and reduced systolic BP (EH, -8.33 mm Hg [CI, -14.55 to -2.12]; <i>P</i>=0.010; hyperaldosteronism, -7.35 mm Hg [CI, -12.69 to -2.01]; <i>P</i>=0.008). To account for early study termination, a conservative significance threshold of α=0.025 was implemented, which all end points crossed.</p><p><strong>Conclusions: </strong>Oral KCl supplementation mobilizes intracellular Na<sup>+</sup> stores, corrects pathological Na<sup>+</sup>/K<sup>+</sup> distribution, and lowers BP across hypertension phenotypes. This safe, targeted approach warrants consideration as a scalable public health strategy for cardiovascular disease prevention.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT06569589.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":""},"PeriodicalIF":18.0000,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Circulation research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1161/CIRCRESAHA.126.329131","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Potassium-enriched table salt lowers blood pressure (BP) and reduces cardiovascular mortality. Whether these beneficial effects stem from reduced Na+ intake, increased K+ intake, or both is unknown. We tested the hypothesis that oral potassium chloride (KCl) supplementation lowers body Na+ content and BP in patients with essential hypertension (EH) or hyperaldosteronism, independent of salt intake.
Methods: Between February 2024 and February 2025, we conducted a single-arm, prospective, longitudinal study with nonrandomized oral KCl intervention in 40 participants with hypertension. All received personalized (blood K+-adjusted) KCl supplementation (Span-K tablets) for 6 to 9 weeks. After the intervention, participants completed a routine diagnostic workup and were classified with EH or hyperaldosteronism. Primary end point: baseline muscle Na+ surplus in hyperaldosteronism. Secondary end point: interventional muscle Na+ mobilization and BP reduction.
Results: Seventeen participants were diagnosed with EH, and 23 with hyperaldosteronism. At baseline, patients with hyperaldosteronism showed higher muscle Na+ content (24.67±2.93 versus 22.48±3.37 mmol/L tissue volume, P=0.023; primary end point). Oral KCl increased 24-hour urine K+ excretion without altering 24-hour urine Na+. KCl supplementation successfully eliminated the muscle Na+ surplus in the hyperaldosteronism group (-1.90 mmol/L tissue volume [CI, -3.20 to -0.60]; P=0.005; secondary end point), lowered blood Na+/K+ ratios in both groups (EH, -5.34 [CI, -7.69 to -2.99]; P=4.6×10-5; hyperaldosteronism, -7.02 [CI, -9.04 to -5.01]; P=2.1×10-8), and reduced systolic BP (EH, -8.33 mm Hg [CI, -14.55 to -2.12]; P=0.010; hyperaldosteronism, -7.35 mm Hg [CI, -12.69 to -2.01]; P=0.008). To account for early study termination, a conservative significance threshold of α=0.025 was implemented, which all end points crossed.
Conclusions: Oral KCl supplementation mobilizes intracellular Na+ stores, corrects pathological Na+/K+ distribution, and lowers BP across hypertension phenotypes. This safe, targeted approach warrants consideration as a scalable public health strategy for cardiovascular disease prevention.
期刊介绍：
Circulation Research is a peer-reviewed journal that serves as a forum for the highest quality research in basic cardiovascular biology. The journal publishes studies that utilize state-of-the-art approaches to investigate mechanisms of human disease, as well as translational and clinical research that provide fundamental insights into the basis of disease and the mechanism of therapies.
Circulation Research has a broad audience that includes clinical and academic cardiologists, basic cardiovascular scientists, physiologists, cellular and molecular biologists, and cardiovascular pharmacologists. The journal aims to advance the understanding of cardiovascular biology and disease by disseminating cutting-edge research to these diverse communities.
In terms of indexing, Circulation Research is included in several prominent scientific databases, including BIOSIS, CAB Abstracts, Chemical Abstracts, Current Contents, EMBASE, and MEDLINE. This ensures that the journal's articles are easily discoverable and accessible to researchers in the field.
Overall, Circulation Research is a reputable publication that attracts high-quality research and provides a platform for the dissemination of important findings in basic cardiovascular biology and its translational and clinical applications.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
