Mineralocorticoid activity and the excretion of an oral potassium load in normal man

Mineralocorticoid activity and the excretion of an oral potassium load in normal man. In six healthy males on a fixed sodium/potassium (Na/K) intake, we studied the relation between plasma K and urine K and Na excretion after an oral K load. Studies were repeated during fludrocortisone (0.5mg bid) or spironolactone (50mg qid), that is, after escape from the Na-retaining and Na-excreting effects of these drugs. A steep positive relation between plasma K (ordinate) and urine Kor Na (abscissa) was found, compatible with a strong influence of changes in plasma K on K and Na excretion. Fludrocortisone reset the relation to a lower level of plasma K. Spironolactone, on the other hand, had little effect on these relations, although a tendency towards a higher plasma K could be recognized. Paradoxically, the K load was excreted less efficiently during fludrocortisone, probably due to enhanced cellular K deposition. Prolonged kaliuresis relative to the transient rise in plasma K and natriuresis was found only without medication. Only in this situation aldosterone rose and fell parallel to plasma K. We conclude that: 1) chronic mineralocorticoid increase shifts the set point of both K and Na excretion following a K load to a lower plasma K, compatible with resetting of the positive influence of plasma K on distal solute delivery towards a lower plasma K; 2) total kaliuresis is paradoxically low due to enhanced cellular K uptake; 3) blockade of endogenous aldosterone action has relatively little influence on these relations between plasma K and urine K or Na; 4) the contribution of acute aldosterone stimulation to the excretion of a single oral K load can be recognized as a delayed kaliuresis extending beyond the peak in plasma K