Does short-term potassium supplementation reduce blood pressure and alter atrial natriuretic peptide in normotensive women?
Short-term potassium supplementation in normotensive women causes a transient fall in systolic blood pressure, likely mediated by increased vasodilator prostanoid synthesis and mild natriuresis, which is counteracted by homeostatic increases in aldosterone and reductions in ANP.
To determine the early effect of potassium loading on blood pressure regulatory mechanisms, the effect of 4 days' supplementation with 80 mmol/day KCl on blood pressure and vasodilator hormone release was examined using a double-blind crossover design in normotensive women with a baseline potassium excretion of 51.8 +/- 2.7 mmol/day. Systolic blood pressure fell 1.7 +/- 0.6 mm Hg, (P less than .01) in association with a mean increase in sodium excretion of 14.7 +/- 4.5 mmol/day and an increase in urine volume of 122.6 +/- 57.0 mL/day. There was a small but significant fall in plasma atrial natriuretic peptide (ANP) over the 4 days of potassium supplementation, while significant increases were seen in the levels of plasma potassium (P less than .01) and aldosterone (P less than .01). After 4 days of KCl, urinary 6-keto-PGF1 alpha was significantly elevated and correlated positively with urinary sodium excretion. Plasma renin activity was unchanged. The results suggest that increased vasodilator prostanoid synthesis and a mild natriuresis may contribute to the transient fall in systolic blood pressure. The increase in aldosterone and reduction in ANP probably represent homeostatic responses to this natriuresis, and could account for the failure of potassium supplementation to induce a long-term reduction in blood pressure in other studies in normotensive subjects.
Barden et al. (Fri,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: