Oral potassium lowers clinic BP in untreated primary hypertension meta-analysis

BackgroundPotassium has biologic plausibility to lower blood pressure (BP) via natriuresis, vascular effects, and RAAS modulation. The clinical effect in untreated primary hypertension remains uncertain. ObjectivesTo estimate the effect of oral potassium supplementation on clinic and 24-h ambulatory BP (ABPM) and to summarize safety. MethodsWe 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. ResultsNineteen 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; I{superscript 2} = 92.3%) and DBP -4.0 mmHg (-6.2 to -1.7; PI -14.1 to 6.1; I{superscript 2} = 94.8%). ABPM effects were smaller and imprecise: SBP -2.4 mmHg (-5.2 to 0.4; I{superscript 2} = 55.0%) and DBP -1.6 mmHg (-4.2 to 1.1; I{superscript 2} = 84.3%). Any adverse event was more frequent (RR 2.41; {approx}40 more per 1000, 17-75), with small absolute increases in total withdrawals (RR 1.32; {approx}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. DiscussionOur 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. ConclusionsIn 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.