Abolished relationship between pancreatic HCO-3secretion and arterial pH during carbonic anhydrase inhibition

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Abstract
After acetazolamide administration, CO2 hydration in [pig] pancreatic cells would be slow and might become a rate-limiting factor to pancreatic HCO32- secretion. Pancreatic HCO3- secretion, normally pH dependent, would become slow and pH-independent. Acetazolamide would not be expected to interfere with the capacity of the secretory mechanism to generate a proton potential gradient between pancreatic cells and interstitial fluid. These predictions were examined in 5 anesthetized, secretin infused (2.7 CU [canine unit]/kg body wt h-1) pigs. Pancreatic juice was collected from a catheter in the pancreatic duct. Arterial pH was varied through i.v. HCl and NaHCO3 infusions and CO2 addition to inspired air. Before acetazolamide, HCO3- secretion varied with plasma pH and averaged 298 .+-. 30 .mu.mol/min at control arterial pH. Acetazolamide (150 mg/kg, i.v.) reduced HCO3- secretion to 84 .+-. 12 .mu.mol/min and rendered secretion independent of arterial pH between pH 7.6 and pH 7.0. Acetazolamide imposes a pH-independent transport maximum on pancreatic HCO3- secretion, but does not reduce the capacity of the secretory mechanism to sustain a proton potential gradient between cells and interstitial fluid.

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