Control of excretion of potassium: lessons from studies during prolonged total fasting in human subjects

Abstract

A deficit of K+ of close to 300 mmol develops in the first 2 wk of fasting, but little further excretion of K+ occurs, despite high levels of aldosterone and the delivery of ketoacid anions that are not reabsorbed in the distal nephron. Our purpose was to evaluate how aldosterone could have primarily NaCl-retaining, rather than kaliuretic, properties in this setting. To evaluate the role of distal delivery of Na+, four fasted subjects recieved an acute infusion of NaCl to induce a natriuresis. To assess the role of distal delivery of [Formula: see text], five fasted subjects were given an infusion containing NaHCO3. The natriuresis induced by an infusion of NaCl caused only a small rise in the rate of excretion of K+ (0.8 ± 0.1 to 1.9 ± 0.3 mmol/h); in contrast, when [Formula: see text]replaced Cl− in the infusate, K+ excretion rose to 8.3 ± 2.2 mmol/h, despite little excretion of[Formula: see text] (urine, pH 5.8) and similar rates of excretion of Na+. The transtubular K+ concentration gradient was 19 ± 3 with [Formula: see text] and 6 ± 2 with NaCl. We conclude that the infusion of NaHCO3 led to an increase in K+ excretion, likely reflecting an increased rate of distal K+secretion. With a low distal delivery of[Formula: see text], aldosterone acts as a NaCl-retaining, rather than a kaliuretic, hormone.