Abstract
Abstract
Metabolic acidosis was induced by NH4Cl ingestion in a normal pigtail macaque (Macaca nemestrina) and a pigtail macaque with an inherited deficiency of red cell carbonic anhydrase I (CA I). After this acid stress, both the normal and CA I-deficient animals were able to acidify their urine, and displayed similar hydrogen ion clearance indexes. These findings suggest that a defective red cell CA I, reported in some cases of renal tubular acidosis in humans, is not directly responsible for the impairment of bicarbonate reabsorption in the kidney tubules.
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