Effect of acetazolamide and parathyroid hormone on HCO3 and PO4 excretion.
It has been recently demonstrated that parathyroid hormone (PTH) inhibits renal cortical carbonic anhydrase. Based on this in vitro study, it was suggested that PTH depresses proximal reabsorption of phosphate and bicarbonate reabsorption in vivo by inhibiting carbonic anhydrase. To test this hypothesis, we measured bicarbonate and phosphate excretion in four groups of dogs. Group I received PTH for 2 hours; group II received acetazolamide for 2 hours; group III received PTH for 2 hours and acetazolamide in the 2nd hour; and in group IV, acetazolamide was given for 2 hours with PTH ADDED IN THE 2ND HOUR. Acetazolamide administration resulted in maximal bicarbonate excretion in the 1st hour and maximal phosphate excretion in the 2nd hour. Addition of acetazolamide to animals receiving PTH or addition of PTH to animals receiving acetazolamide resulted in additional increases in bicarbonate and phosphate excretion. These data demonstrate that PTH induces bicarbonate and phosphate excretion regardless of whether carbonic anhydrase is intact or nearly 100% inhibited by acetazolamide. These data do not support the hypothesis that PTH inhibits bicarbonate and phosphate reabsorption by inhibiting carbonic anhydrase.
D000086:Acetazolamide / Q000494:pharmacology*; D000818:Animals; D001639:Bicarbonates / Q000097:blood / Q000652:urine*; D004285:Dogs; D004347:Drug Interactions; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects; D010281:Parathyroid Hormone / Q000494:pharmacology*; D010710:Phosphates / Q000097:blood / Q000652:urine*; D012964:Sodium / Q000652:urine; D013997:Time Factors
D001639:Bicarbonates; D010281:Parathyroid Hormone; D010710:Phosphates; D012964:Sodium; D000086:Acetazolamide