Gijsbers · Journal of human hypertension 2015 · randomized, placebo-controlled crossover trial · n=37

Effects of sodium and potassium supplementation on blood pressure and arterial stiffness: a fully controlled dietary intervention study.

Cited 69 times in the scientific literature.

Level 2 - randomized trial

Individual randomized, placebo-controlled crossover trial

PubMed 25673113 · doi:10.1038/jhh.2015.3 · record verified 2026-08-29

What was done

A randomized, placebo-controlled crossover trial evaluated the effects of sodium and potassium supplementation on blood pressure and arterial stiffness in 37 untreated prehypertensive or hypertensive individuals (36 completed; baseline blood pressure 145/81 mm Hg). Participants were maintained on a fully controlled diet low in sodium and potassium. Following a 1-week run-in, subjects received 4-week treatments in random order: sodium capsules (3 g/day, equivalent to 7.6 g/day salt), potassium capsules (3 g/day), or placebo. Fasting office blood pressure, 24-hour ambulatory blood pressure, pulse wave velocity, and augmentation index were measured at baseline and after each 4-week period.

What was found

Active supplementation increased 24-hour urinary sodium excretion by 98 mmol and potassium excretion by 63 mmol compared to placebo. Sodium supplementation significantly increased office blood pressure (+7.5/3.3 mm Hg), 24-hour blood pressure (+7.5/2.7 mm Hg), and central blood pressure (+8.5/3.6 mm Hg). Potassium supplementation significantly decreased 24-hour blood pressure (-3.9/1.6 mm Hg) and central pulse pressure (-2.9 mm Hg). Neither sodium nor potassium supplementation significantly altered pulse wave velocity or augmentation index.

Why it matters

Using fully controlled feeding, this study confirms that supplemental sodium substantially raises blood pressure, while potassium supplementation reduces ambulatory blood pressure even on top of a baseline low-sodium diet.

Limits

The study was small (36 completed subjects) and short in duration (4 weeks per phase), which may be inadequate to detect structural changes in arterial stiffness. The highly controlled dietary environment may not reflect real-world, free-living dietary compliance.

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