TISSUE AND RENAL RESPONSE TO CHRONIC RESPIRATORY ACIDOSIS*

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Abstract
Urinary acid excretion (NH3 plus titratable acid) increased transiently for the first day or two and then returned to control values despite continued severe respiratory acidosis. A slight rise in urine pH, presumably due to increased bicarbonate excretion as serum bicar- bonate reached maximal values, appeared to be chiefly responsible for the rapid return of urinary ammonia to control values. Renal glutaminase was not activated during respiratory acidosis; this is strong evidence against the role of intracellular or extracellular pH as regulatory fac- tors in the adaptation of renal ammonia-producing enzymes. In spite of increased tubular bicarbonate reabsorption, as evidenced by the stabilization of serum bicarbonate at high levels, adaptation of renal carbonic anhydrase did not occur. Cl excretion was greatly elevated the 1st day of respiratory acidosis but thereafter returned to control values. K excretion was also markedly elevated the 1st day and con-tinued to be excreted at a slightly increased rate for the remainder of the study. Muscle Na and K were slightly decreased after 11 days of respiratory acidosis. The most striking change in bone electrolytes was a fall in Mg content.

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