Key result
Oral potassium supplementation lowers clinic SBP by ~7 mmHg in untreated primary hypertension.
Why the study?
Although potassium has biologic plausibility to lower blood pressure via natriuresis, vascular effects, and RAAS modulation, the clinical effect and safety of oral potassium supplementation in adults with untreated primary hypertension remained uncertain.
Does oral potassium supplementation lower clinic and 24-hour ambulatory blood pressure in adults with untreated primary hypertension?
Meta-Analysis (n=803)
Most often double-blind, with a minority open-label or single-blind
Randomized trials (14 crossover, 5 parallel)
Yes
Does oral potassium supplementation lower clinic and 24-hour ambulatory blood pressure in adults with untreated primary hypertension?
In adults with untreated primary hypertension, oral potassium supplementation produces modest, clinically relevant reductions in clinic blood pressure (−7.2/−4.0 mmHg) with mostly mild gastrointestinal adverse events, though 24-hour ambulatory blood pressure effects are smaller and uncertain.
Supports potassium supplementation for clinic BP lowering in untreated hypertension; extends RCT meta-analyses while leaving ambulatory effects imprecise.
Background Potassium has biologic plausibility to lower blood pressure (BP) via natriuresis, vascular effects, and RAAS modulation. The clinical effect in untreated primary hypertension remains uncertain. Objectives To estimate the effect of oral potassium supplementation on clinic and 24-h ambulatory BP (ABPM) and to summarize safety. Methods We included randomized trials (parallel or crossover) in adults (≥18 y) with untreated primary hypertension comparing oral potassium supplements vs placebo, sodium chloride, or no treatment. Trials without end-of-treatment BP or without performed 24-h urinary potassium measurements were excluded. Sources: PubMed, Embase, CENTRAL, Scopus, CINAHL, trial registries (through Jan 31, 2025; updated Oct 1, 2025). Random-effects meta-analyses (REML, Knapp–Hartung) pooled end-of-treatment mean differences (mmHg) and risk ratios (RR); prediction intervals (PI) were reported. Certainty was appraised with GRADE. Results Nineteen trials (803 participants; 14 crossover, 5 parallel; median duration 4 weeks) met criteria. Potassium lowered clinic BP: SBP −7.2 mmHg (95% CI −11.1 to −3.4; PI−24.5 to 10.1; I² = 92.3%) and DBP −4.0 mmHg (−6.2 to −1.7; PI −14.1 to 6.1; I² = 94.8%). ABPM effects were smaller and imprecise: SBP −2.4 mmHg (−5.2 to 0.4; I² = 55.0%) and DBP −1.6 mmHg (−4.2 to 1.1; I² = 84.3%). Any adverse event was more frequent (RR 2.41; ≈40 more per 1000, 17–75), with small absolute increases in total withdrawals (RR 1.32; ≈4 more per 1000, 0–9) and AE-related withdrawals (RR 1.28; 0–10 more per 1000). Signals suggested larger benefits with higher baseline BP, longer duration, and in parallel-group trials. Discussion Our findings reinforce the physiological plausibility that potassium exerts antihypertensive effects primarily through natriuresis and vascular modulation, rather than a simple dose-dependent mechanism. The modest mean effect, together with wide prediction intervals, underscores the role of individual sodium–potassium balance, baseline BP, and intervention duration in determining response. These data support a shift from universal supplementation toward context-specific implementation, guided by biochemical monitoring and patient characteristics. Conclusions In untreated primary hypertension, oral potassium supplementation yields modest, clinically relevant reductions in clinic BP, while ABPM effects are smaller and very uncertain. Given mostly mild AEs and small absolute increases in withdrawals, supplementation may be conditionally considered alongside sodium reduction and routine laboratory monitoring. Adequately powered parallel trials (≥8–12 weeks) with prespecified ABPM and standardized safety reporting are needed.
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Ashiyama et al. (2026) conducted a meta-analysis in Untreated primary hypertension (n=803). Oral potassium supplementation (predominantly potassium chloride, also citrate, aspartate, bicarbonate, or gluconate) vs. Placebo (16/19 trials), no treatment (2/19 trials), or sodium chloride (1/19 trials) was evaluated on End-of-treatment clinic systolic blood pressure (SBP, mmHg) (MD -7.2 mmHg, 95% CI -11.1 to -3.4). Oral potassium supplementation lowered clinic systolic blood pressure by 7.2 mmHg (95% CI -11.1 to -3.4) and diastolic blood pressure by 4.0 mmHg (-6.2 to -1.7) in untreated primary hypertension.
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