Effects of parathyroid hormone and calcitonin on electrolyte excretion in the rabbit

Abstract

We evaluated the effects of bovine parathyroid hormone (PTH) and salmon calcitonin on urinary electrolyte excretion in thyroprathyroidectomized rabbits and rats in vivo to obtain data for the isolated rabbit tubule in vitro. In rats, PTH increased fractional phosphate excretion (FE(PO4)) in a dose-dependent fashion from 0.13±0.02% to 36.0±3.0%. In rabbits, FE(PO4) started at a much higher level, 18.0±4.0%, and increased to 28.0±4.0% with pharmacologic doses of PTH. In rats, PTH significantly decreased calcium excretion at the lowest dose, and this effect persisted at the higher doses. In rabbits, calcium excretion was markedly higher and was significantly decreased at the highest dose of PTH. In rats, calcitonin increased FE(PO4), at low dose levels without further increases at the higher dose. In contrast, calcitonin was not phosphaturic in rabbits, and at the highest dose FE(PO4) was significantly decreased. In rats, calcitonin increased FE(Na) from 0.2±0.1% to 1.6±0.5% at the highest dose. In rabbits, calcitonin was markedly natriuretic; FE(Na) increased from 4.0±0.5% to 18.0±3.0% at the low dose without further increases at the higher dose. FE(Cl) increased in parallel from 6.0±0.6% to 23.0±4.0%. Thus, PTH resulted in similar directional changes in phosphate and calcium handling in both rabbit and rat. The magnitude of response, however, varied between species. The predominant effects of calcitonin were to increase phosphate excretion in the rat and sodium chloride excretion in the rabbit.