The effect of acetazolamide on collecting duct H+ secretion was studied by measuring the ability of dogs to generate a high urine-to-blood (U-B) pCo2 gradient. In hydropenic dogs, acetazolamide administration resulted in a significant increase in urine pCO2 to the same levels seen in HCO3-loaded dogs with comparable urine HCO3 concentrations. Acetazolamide administration to HCO3-loaded dogs failed to cause a decrease in U-B pCO2. Administration of tris(hydroxymethyl)aminomethane (Tris) buffer to these dogs resulted in a significant increase in U-B pCO2 to the same level as that seen in normal HCO3-loaded dogs receiving Tris. Administration of acetazolamide to dogs with moderately alkaline urine (urine pH 6.4-7.4) failed to either lower or prevent the increase in U-B pCO2 caused by neutral phosphate infusion. These data demonstrate that acetazolamide does not impair the generation of high U-B pCO2. We suggest that the ability to generate a normal U-B pCO2 gradient in the presence of acetazolamide is the result of CO2 generation via uncatalyzed H+ secretion coupled with a decrease in tubular permeability to CO2 also induced by carbonic anhydrase inhibition.
|Original language||English (US)|
|Number of pages||11|
|Journal||Mineral and Electrolyte Metabolism|
|State||Published - Jan 1 1981|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism