1. The excretion of structural analogues of ammonia in acidic and alkaline urine was investigated. The lipid-soluble compounds n-propylamine, n-butylamine and n-amylamine and the water-soluble compounds hydrazine and methylhydrazine resemble ammonia in being more rapidly excreted in acidic urine. By contrast, the excretion of the water-soluble amines methylamine and ethylamine is unaffected by changes in urinary pH.

2. Arguments are advanced, based on the results, that pH-dependent excretion of ammonia is due to diffusion of the water-soluble un-ionized fraction through the aqueous phase of the cell membrane, and the same applies to the hydrazines. However that of n-propylamine and the higher-molecular-weight alkylamines is due to diffusion through the lipid phase of the cell membrane. The data suggest that this latter form of diffusion is the more rapid one.

3. After injection of glutamyl-γ-methylamide and the corresponding ethylamide, both methylamine and ethylamine excretions are significantly higher in acidosis, rising further in chronic acidosis. This indicates that the glutaminase II pathway of ammonia genesis increases in activity in the acidotic rat in vivo.

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