Abstract
In acute experiments on anesthetized dogs, renal excretion of titratable acid was measured during maintenance of high levels of urinary buffer excretion. Acute respiratory acidosis was induced with 12% CO2 and acute respiratory alkalosis by hyperventilation with a respiration pump. The excretion of titratable acid increased during respiratory acidosis and decreased during respiratory alkalosis. Measurements during recovery periods revealed that the effects of respiratory acidosis were rapidly reversible, while respiratory alkalosis produced a lasting depression of the tubular capacity to secrete hydrogen ions. Ammonia excretion showed only small and irregular changes, although it usually increased in respiratory acidosis and decreased during respiratory alkalosis. The results are interpreted in terms of total hydrogen ion secretion by the renal tubules, and it is concluded that respiratory acidosis and alkalosis exert their renal effects by influencing the availability of carbonic acid, and therefore of hydrogen ions, inside the tubular cells.
Published Version
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