Urinary pCO2 during carbonic anhydrase inhibition in the dog

H. Rubinstein, D. C. Batlle, M. Roseman

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

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 languageEnglish (US)
Pages (from-to)49-59
Number of pages11
JournalMineral and Electrolyte Metabolism
Volume5
Issue number1
StatePublished - Jan 1 1981

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry

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