Acute effect of calcitonin on rat renal electrolyte transport.

Renal clearance studies were performed on parathyroid-intact and acutely thyroparathyroidectomized (TPTX) rats to clarify calcitonin (CT) action on renal electrolyte transport. Although CT (0.15 U x 100 g body wt-1 x h-1) reduced fractional excretion of calcium and magnesium by 72 and 46%, respectively, in TPTX rats without altering sodium and phosphate excretion, a 10-fold increase in CT (1.5 U) caused a smaller reduction in calcium and magnesium excretion and significantly increased sodium and phosphate excretion. A higher CT dose (15 U) did not alter calcium excretion, increased magnesium excretion, and caused an even greater increase in sodium and phosphate excretion. Results in parathyroid-intact animals were similar. Despite the fall in plasma calcium following CT administration, the filtered calcium load was unaltered due to a concomitant increase in glomerular filtration rate. Calcium infusion prior to CT (0.15 U) prevented a detectable fall in plasma calcium concentration. However, a 45% fall in fractional calcium excretion occurred despite the significant increase in filtered calcium. These data suggest that the physiological role of calcitonin on the nephron is to conserve calcium. Reports of increased electrolyte excretion presumably reflect a depressant effect of pharmacological doses of CT on nephron function.