In mice given a 25 mg deoxycorticosterone acetate (DOCA) pellet plus 1% NaCl in drinking water, blood pressure rose by day 2, when the animals had lost body potassium and water but had not yet retained sodium. Kidneys conserved free water despite higher fluid intake, a sign of intracellular dehydration. Sodium retention came later (days 6 and 12), replacing lost potassium. Sodium bicarbonate produced a similar sodium/potassium redistribution without early dehydration or salt-sensitive pressure rises. Oral potassium supplementation corrected both dehydration and blood pressure.
This evidence comes from mice, so it is hypothesis-generating rather than practice-changing. The DOCA model is a severe mineralocorticoid-excess state that mimics primary aldosteronism more than common essential hypertension, and the sodium-overload paradigm remains well supported by human feeding trials such as DASH-Sodium. Still, the paper fits a growing body of human data pointing to potassium as the underappreciated half of the sodium story: higher potassium intake lowers blood pressure and stroke risk in meta-analyses, and potassium-enriched salt substitutes cut cardiovascular events in the SSaSS trial of about 21,000 Chinese adults. The mouse data offer a possible mechanism, in which potassium depletion triggers water conservation, with sodium retention as a secondary response. For adults, the practical message is unchanged and consistent with this work: favour potassium-rich foods such as legumes, vegetables, fruit and potatoes alongside sodium reduction. Anyone with kidney disease or taking potassium-sparing drugs or ACE inhibitors should consult a physician before raising potassium. Interesting mechanistic reframing, but incremental until human studies test it.