Ammonia buffer

Ammonia buffer

Most ammonia (60%) is synthesized in proximal tubule cells by deamidation and deamination of the amino acid glutamine [rest comes from glycine and alanine].

Ammonia is secreted into the urine by two mechanisms.

1.   As NH₃ (because of its lipid soluble nature), it diffuses into the tubular urine; as NH₄ ⁺, it substitutes for H⁺ on the Na⁺/H⁺ exchanger. In the lumen, NH₃ combines with secreted H⁺ to form NH₄⁺, which is excreted [because of its polar nature and therefore can not diffuse back into the tubular epithelium].

For each mEq of H⁺ excreted as NH₄⁺, one mEq of new HCO₃^_ is added to the blood. The hydration of CO₂ in the tubule cell produces H⁺ and HCO₃ ^_.

2.   Two H⁺s are consumed when the anion α₂-ketoglutarate^2_ is converted into CO₂ and water or into glucose in the cell. The new HCO₃^_ returns to the blood along with Na⁺.

If excess acid is added to the body, urinary ammonia excretion is increased for two reasons.

·        More acidic urine traps more ammonia (as NH₄⁺) in the urine.

·        Renal ammonia synthesis from glutamine increases over several days which is a lifesaving adaptation because it allows the kidneys to remove large H⁺ excesses and add more new HCO₃^_ to the blood. With severe metabolic acidosis, ammonia excretion may increase almost 10-fold.

Renal ammonia synthesis is increased through an increase in the glutaminase activity.