Sodium wasting in potassium depletion: the role of aldosterone.

Impaired renal conservation of sodium (Na) has been reported in potassium (K)-depleted humans and experimental animals when challenged with sodium restriction(l-3); however, the magnitude, duration, or mechanism of this phenomenon have never been clearly defined. It is known that potassium depletion depresses aldosterone secretion and that sodium restriction stimulates it(l,4-7). Johnson et al.(l) have reported transient sodium wasting in potassium-depleted humans after sodium restriction. Urinary aldosterone excretion was markedly depressed at the time of maximum sodium wasting and was elevated by the time sodium balance had spontaneously returned to normal. Cannon(4) reported similar results. These studies suggest that the impairment of sodium conservation in potassium depletion might be the result of depressed aldosterone secretion which accompanies potassium depletion. It is significant that impaired sodium conservation associated with potassium depletion has been reported only in the face of severe sodium restriction. Potassium depletion in the presence of adequate sodium intake results in sodium retention with excess sodium accumulating in cells and extracellular fluid(1,3,8-10). Hollander(l 1) has suggested that the apparent defect in renal sodium conservation might well be explained by the excretion of the higher