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| Item Type: | Article |
|---|---|
| Title: | Oral KCl supplementation safely reduces body Na(+) surplus and blood pressure |
| Creators: |
Marton, Adriana, Tran, Hieu T.N., Morisawa, Norihiko, Osman, Ismail, Saffari, Seyed Ehsan, Lim, Tzy Tiing, Yam, Wan Keat, Chuah, Matthew B., Tay, Wei Lin, Moy, Wai Lun, Khong, Pek-Lan, Chin, Calvin W.L., Nagel, Armin M., Foo, Roger S.Y., Luft, Friedrich C.  ORCID: https://orcid.org/0000-0002-8635-1199, Finkelstein, Eric, Kovalik, Jean-Paul, Rauh, Manfred, Puar, Troy and Titze, Jens
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| Abstract: | BACKGROUND: Potassium(-5)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(-5)arm, prospective, longitudinal study with nonrandomized oral KCl intervention in 40 participants with hypertension. All received personalized (blood K(+)(-5)adjusted) KCl supplementation (Span(-5)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(-5)hour urine K(+) excretion without altering 24(-5)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)5; hyperaldosteronism, −7.02 [CI, −9.04 to −5.01]; P=2.1×10((-5)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. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT06569589. |
| Keywords: | Angiotensins, Blood Pressure, Hypertension, Potassium, Sodium |
| Source: | Circulation Research |
| ISSN: | 0009-7330 |
| Publisher: | American Heart Association |
| Date: | 28 September 2026 |
| Official Publication: | https://doi.org/10.1161/circresaha.126.329131 |
| PubMed: | View item in PubMed |
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