We examined the effect of
parathyroid hormone (PTH), administrated for 24-48 h, on
acid-base homeostasis in dogs. Parathyroid extract (PTH), 15 IU/kg/day, given subcutaneously, caused metabolic
alkalosis (control vs. experimental; mean +/- SEM): plasma HCO3, 21.3 +/- 0.3 vs. 24.2 +/- 0.5 mEq/l (p less than 0.001); plasma H+, 37.7 +/- 1.1 vs. 35.7 +/- 1.4 nEq/l (p less than 0.05), and net
acid excretion, 48.6 +/- 2.0 vs. 65.1 +/- 4.0 mmol/day (p less than 0.01). PTH administered by continuous
intravenous infusion had similar effects (control vs. experimental): plasma HCO3, 21.4 +/- 0.4 vs. 23.6 +/- 0.7 mEq/l (p less than 0.001) and net
acid excretion, 54.0 +/- 3.5 vs. 68.3 +/- 5.7 mmol/day (p less than 0.05). PTH, 8 IU/kg/day, had qualitatively similar but quantitatively less profound consequences. Bicarbonaturia was not observed in any group. The effects of PTH were similar in adrenalectomized dogs maintained on
hormone replacement.
Indomethacin (150 mg/day) prevented the renal effects of PTH so that no increase in net
acid secretion occurred. However, metabolic
alkalosis still developed: control vs. experimental plasma HCO3, 21.8 +/- 0.5 vs. 23.9 +/- 0.5 mEq/l (p less than 0.001).
Dichloromethanediphosphonate blunted both the renal and nonrenal effects of PTH, such that
hypercalcemia, metabolic
alkalosis and increased net
acid excretion were quantitatively less and delayed in onset. In summary, PTH administration for 24-48 h causes metabolic
alkalosis in dogs, the result of renal and nonrenal mechanisms.