PARATHYROID-HORMONE-INDUCED METABOLIC ALKALOSIS IN DOGS

  • 1 January 1982
    • journal article
    • research article
    • Vol. 8  (2) , 78-91
Abstract
The effect of parathyroid hormone (PTH), administered for 24-48 h, on acid-base homeostasis in dogs was examined. Parathyroid extract (PTH), 15 IU/kg per day, given. s.c., caused metabolic alkalosis (control vs. experimental; mean .+-. standard error of the mean): plasma HCO3, 21.3 .+-. 0.3 vs. 24.2 .+-. 0.5 meq/l (P < 0.001); plasma H+, 37.7 .+-. 1.1 vs. 35.7 .+-. 1.4 neq/l (P < 0.05), and net acid excretion, 48.6 .+-. 2.0 vs. 65.1 .+-. 4.0 mmol/day (P < 0.01). PTH administered by continuous i.v. infusion had similar effects (control vs. experimental): plasma HCO3, 21.4 .+-. 0.4 vs. 23.6 .+-. 0.7 meq/l (P < 0.001) and net acid excretion, 54.0 .+-. 3.5 vs. 68.3 .+-. 5.7 mmol/day (P < 0.05). PTH, 8 IU/kg per 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 < 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. PTH administration for 24-48 h apparently causes metabolic alkalosis in dogs, the result of renal and nonrenal mechanisms.