CONTROL OF EXCRETION OF POTASSIUM - LESSONS FROM STUDIES DURING PROLONGED TOTAL FASTING IN HUMAN-SUBJECTS

A deficit of K+ of close to 300 mmol develops in the first 2 wk of fas ting, but little further excretion of K+ occurs, despite high levels o f aldosterone and the delivery of ketoacid anions that are not reabsor bed in the distal nephron. Our purpose was to evaluate how aldosterone could have primarily NaCl-retaining, rather than kaliuretic, properti es in this setting. To evaluate the role of distal delivery of Na+, fo ur fasted subjects recieved an acute infusion of NaCl to induce a natr iuresis. To assess the role of distal delivery of HCO3-, five fasted s ubjects were given an infusion containing NaHCO3. The natriuresis indu ced by an infusion of NaCl caused only a small rise in the rate of exc retion of K+ (0.8 +/- 0.1 to 1.9 +/- 0.3 mmol/h); in contrast, when HC O3- replaced Cl- in the infusate, K+ excretion rose to 8.3 +/- 2.2 mmo l/h, despite little excretion of HCO3- (urine, pH 5.8) and similar rat es of excretion of Na+. The traustubular K+ concentration gradient was 19 +/- 3 with HCO3- and 6 +/- 2 with NaCl. We conclude that the infus ion of NaHCO3 led to an increase in K+ excretion, likely reflecting an increased rate of distal K+ secretion. With a low distal delivery of HCO3-, aldosterone acts as a NaCl-retaining, rather than a kaliuretic, hormone.