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Am J Physiol 206: 409-414, 1964;
0002-9513/64 $5.00
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Mechanism of lysine-induced kaliuresis

W. Gordon Walker 1, Herbert Dickerman 1, and Luis J. Jost 1

1 Department of Medicine, The Johns Hopkins University and Hospital, Baltimore, Maryland

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.

Key Words: renal tubular K secretion • bicarbonate excretion • bicarbonate excretion and lysine-induced kaliuresis • acidosis and K excretion • extracellular pH and lysine infusion • intracellular K and lysine • cellular penetration of lysine • pCO2 and bicarbonate reabsorption

Submitted on June 19, 1963







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Copyright © 1964 by the American Physiological Society.