Pooling 19 randomized trials (803 adults with untreated primary hypertension, median duration four weeks), oral potassium supplementation lowered clinic blood pressure by 5.3 mm Hg systolic (95% CI 4.4-6.3) and 4.5 mm Hg diastolic versus placebo, sodium chloride, or no treatment. Twenty-four-hour ambulatory reductions were smaller, at 2.8 mm Hg systolic and 3.2 mm Hg diastolic. Adverse events occurred more often with potassium (12.8% versus 3.2%), though withdrawals were uncommon. Heterogeneity was substantial.
The gap between clinic and ambulatory readings is the most instructive detail. Ambulatory pressure tracks cardiovascular risk more faithfully than office readings, and a roughly 3 mm Hg drop is real but modest, closer to what a moderate sodium reduction delivers than to what a first-line antihypertensive achieves. The clinic figure likely overstates the benefit, since short crossover trials and white-coat effects inflate office differences. Population data suggest even small sustained systolic reductions lower stroke risk, which keeps the finding meaningful. The 12.8% adverse-event rate, probably mostly gastrointestinal upset, deserves attention, and supplementation carries hyperkalemia risk in people with kidney disease or those taking ACE inhibitors, ARBs, or potassium-sparing diuretics. Four-week trials say nothing about long-term outcomes. Practically, the evidence favors raising dietary potassium through vegetables, legumes, and fruit, and discussing supplements with a physician first. This is confirmatory rather than paradigm-shifting: it reinforces known potassium-pressure biology while tempering enthusiasm about its size.