The relation between plasma concentrations of glutamine and glycine and utilization of their nitrogens as sources of urinary ammonia.

Abstract

The infusion of a number of amino acids into a peripheral vein or renal artery increases the rate of urinary excretion of ammonia in acidotic dogs (1-3). According to Lotspeich (4), amino acids fall into three groups: those that greatly augment the excretion of ammonia, such as glutamine, as-paragine, alanine, and histidine; those that mod-erately augment the excretion of ammonia, such as glycine, leucine, aspartic acid, and methionine; and those that do not appreciably affect the excretion of ammonia, such as glutamic acid, lysine, and ar-ginine. The inference that those amino acids that increase the excretion of ammonia when infused intravenously are the immediate precursors of uri-nary ammonia under normal conditions is not necessarily correct, for blood ammonia increases sharply when amino acids are infused at the high rates employed in many of these studies (5). Thus a part of the increased urinary ammonia might be derived from preformed ammonia pro-duced elsewhere and delivered to the kidneys in the arterial blood. Furthermore the renal tubular precursor of ammonia, which is utilized in in-creased quantity, might not be solely the amino acid infused but, in part, another formed at some extrarenal site by transamination. A further pos-sible complication is a reduction in the utilization of the nitrogen of one precursor, e.g., glutamine, when the plasma concentration of another pre-cursor, e.g., glycine or alanine, is increased. It is known that certain amino acids compete in renal