Abstract
The infusion of the cationic amino l-lysine, l-arginine, or l-ornithine into dogs regularly increases potassium excretion to levels that exceed the filtered load of potassium. Hyperkalemia occurs during the amino acid infusion as a result of displacement of the intracellular potassium by the cationic amino acids. This rise in plasma K is not necessary for the stimulation of K secretion since infusion of the lysine directly into the renal artery produces K secretion without significant change in plasma K. This increased potassium excretion is promptly suppressed by the administration of thiomerin. The effects upon renal K handling in these experiments appear to be the result of facilitation of tubular secretion of K rather than inhibition of reabsorption.
Published Version
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