CHRONIC CALCITONIN ADMINISTRATION AND RENAL CALCIUM-TRANSPORT IN THE RAT

1. While calcitonin (CT) has now been clearly demonstrated to be a ren al Ca2+-conserving hormone and may share similar transport mechanisms with parathyroid hormone (PTH), the effect of prolonged CT exposure on renal Ca2+ transport has not been evaluated, 2. Consequently, a subma ximal and maximal Ca2+-conserving concentration of human CT was infuse d into groups of anaesthetized acutely thyroparathyroidectomized rats that had been treated with twice daily subcutaneous human (h) CT at a low or high dose or vehicle for 12 days, 3. The maximal hCT infusion ( 10 mu g bolus and per hour) produced a marked inhibitory effect on ren al Ca2+ excretion in vehicle-treated rats, with the fractional excreti on rate of Ca2+ being reduced from 4.49+/-0.31 to 1.39+/-0.23 % (P<0.0 01). However, in rats pretreated with high concentrations of hormone ( 0.25 mu g hCT) twice daily for 12 days, marked Ca2+ conservation was m easured (fractional excretion 1.09+/-0.18%), which was not altered by the additional intravenous administration of maximal hCT 4. Renal Mg2 transport was similarly altered by hCT administration, without any ev idence that prolonged CT inhibited renal Mg2+ transport, The increase in glomerular filtration rate caused by hCT also appeared to persist w ith repeated hormone administration, The fractional excretion of Na+ a nd PO4 was significantly increased by high-but not low-dose hCT treatm ent and was not altered by the addition of a maximal hormone dose at d ay 12, 5. The present study failed to demonstrate any down-regulation of the response to prolonged hCT administration when renal Ca2+ and Mg 2+ transport was measured, If renal escape does occur with CT, as has been suggested but not proven with PTH, other mechanisms, such as horm one production or release, may be responsible.