Natriuretic and kaliuretic response to potassium load: modulation by sodium intake.

Potassium (K) loading is followed by a rapid increase in sodium (Na) and K excretion. To evaluate the influence of Na intake on this effect, we studied the acute natriuretic and kaliuretic response to a single oral K load (100 mmol) in six healthy volunteers equilibrated on a 10-, 100-, and 400-mmol Na intake. Compared to the 100-mmol Na intake, the 400-mmol Na intake greatly enhanced the natriuretic effect of the K load; during the 10-mmol Na intake no natriuresis but even some Na retention occurred. The kaliuretic effect was not significantly changed and occurred at similar values of plasma K. Plasma aldosterone was suppressed during the 400-mmol Na diet and stimulated during the 10-mmol Na diet, but the relative increments after the KCl load did not differ among the three diets. In conclusion, whereas the effect of a K load on kaliuresis is relatively independent of Na intake, its effect on Na excretion varies from marked natriuresis to slight Na retention. The Na retention is probably due to acute K-induced aldosterone stimulation, and the natriuresis to K-induced increase in distal Na delivery not utilized to promote K excretion. Apparently, the integration of renal Na and K handling after a K load is such that K balance is maintained at the cost of Na balance.