Mechanism of lysine-induced kaliuresis

Abstract

Kaliuresis induced by the intravenous infusion of l-lysine monohydrochloride persists when experiments are done in the presence of pre-existing metabolic acidosis produced by NH4Cl administration. The relation between lysine-induced kaliuresis and the rate of urinary sodium excretion indicates that the K excretion is quite sensitive to changes in sodium excretion when sodium excretory rates are low but this relation tends to disappear at high rates of sodium excretion. Thus the final mechanism whereby K enters the urine in these experiments appears to be sodium-for-potassium exchange. Increasing infusion rates of l-lysine monohydrochloride result in the appearance of an alkaline urine despite a progressive extracellular metabolic acidosis. Under these conditions the rate of bicarbonate excretion may exceed 80% of the amount of bicarbonate filtered. The data are best explained by postulating the l-lysine monohydrochloride infused at pH 7.4 produces an extracellular acidosis and intracellular alkalosis, thereby suppressing the kidney's ability to secrete H+ ion and facilitating K+ secretion.