Potassium supplementation ameliorates mineralocorticoid-induced sodium retention

Potassium supplementation ameliorates mineralocorticoid-induced sodium retention. Potassium depletion induced by dietary potassium restriction causes sodium retention while potassium supplementation augments urinary sodium excretion. The role of external potassium balance in modulating mineralocorticoid-induced sodium retention in humans is unknown. Accordingly, eight healthy subjects were studied at the Clinical Research Center receiving a constant diet providing (per kg body wt) sodium 2.5 mmol, potassium 1.1 mmol daily. After establishing basal sodium and potassium balance over three days, each subject received 9α-fludrocortisone 0.4 mg/day for 10 days. Subjects were studied twice, four to eight weeks apart, in a double blind, randomized crossover design receiving either placebo or additional KC1 (80 mmol/day) over the 10 day study period. Serum potassium concentrations were unchanged from basal values on KCl while the values fell (4.1 ± 0.1 vs. 3.4 ± 0.1 mmol/liter, P = 0.01) on placebo. Urinary sodium excretion decreased with fludrocortisone administration in both groups, but this decrease reached significance only in the placebo group. Furthermore, during fludrocortisone administration the sodium excretion rates on KCl were significantly higher compared to the values noted on placebo (134 ± 8 vs. 112 ± 13 mmol/day, P = 0.01). Body weight recorded after 10 days of fludrocortisone administration was higher on placebo compared to KC1 (72.3 ± 2.8 vs. 71.6 ± 2.8 kg, P = 0.01). Plasma renin activity, and aldosterone concentrations decreased on fludrocortisone while atrial natriuretic peptide levels increased. These studies suggest that amelioration of hypokalemia attenuates mineralocorticoid-induced sodium retention. Therefore, potassium depletion may contribute to the mineralocorticoid-induced sodium retention