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 9 alpha-
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 KCl (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 KCl (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.