In a 40-participant prospective study of adults with essential hypertension or hyperaldosteronism, personalised oral KCl supplementation (Span-K tablets, 6–9 weeks) reduced systolic blood pressure by approximately 8 mmHg in both groups (EH: −8.33 mmHg, P=0.010; hyperaldosteronism: −7.35 mmHg, P=0.008). Crucially, 24-hour urinary sodium excretion did not change, confirming the effect was not driven by reduced salt intake. Instead, KCl mobilised intracellular sodium stored in muscle tissue — a surplus that was measurably higher in hyperaldosteronism patients at baseline — and corrected pathological blood Na⁺/K⁺ ratios substantially in both groups.
This finding reframes the cardiovascular benefit of potassium-enriched salt substitutes: rather than merely displacing sodium at the dinner table, potassium appears to actively pull sodium out of tissue depots. That mechanism aligns with the sodium-buffering role of skin and muscle glycosaminoglycans, an area that has grown considerably since the Titze laboratory's foundational work on non-osmotic sodium storage. For adults managing hypertension, an ~8 mmHg systolic drop from a supplement alone rivals the effect of a single antihypertensive drug class and is clinically meaningful for cardiovascular and stroke risk reduction.
Limitations are notable: the study is small, non-randomised, and lacks a placebo arm, making causality provisional. Early termination required a tightened significance threshold. Larger randomised trials are essential before this becomes routine clinical guidance, but the mechanistic precision and effect magnitude make this more than incremental — it is a genuine candidate for rethinking population-level sodium reduction strategies.