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Renal compensation of respiratory acidosis and alkalosis

It is established that the degree of reabsorption of HC0₃~ by the cells of renal tubules is directly proportional to PC0₂ of blood. This reaction does not depend on blood pH. Mechanism of this process is associated with elevation of blood PC0₂ and increase of PC0₂ in tissues.

A process of hydration of carbon dioxide inside the cells of renal tubules increases, and the inflow of H⁺-ions into tubular urine intensifies in exchange for Na⁺-ions. Here, Na⁺ binds with HC0₃" and leaves for blood.

A) Compensation of respiratory alkalosis:

The essence of respiratory alkalosis lies in the decrease of PC0₂ and concentration of HCCyions in blood. A decrease of blood PC0₂ leads to inhibition of C0₂ hydrogenation in the cells of renal tubules and to a decrease of bicarbonate reabsorption from the urine. A lot of bicarbonate remains in the urine and it acquires an alkaline reaction. The concentration of bicarbonate in plasma drops.

B) Compensation of respiratory acidosis:

The process of development of respiratory acidosis is associated with elevation of PC0₂ and increase of the number of HC0₃"ions in blood. Carbon dioxide, entering inside the cells, is hydrogenized:

H⁺ ions are released into tubular urine in exchange for Na⁺ that is being bound inside the cells with HC0₃~ and enters the blood. Retention of bicarbonate in blood leads to chlorine substitution that is excreted with urine.

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