Abstract

The influence of calcitonin (CT) on parathyroid hormone-induced changes in plasma phosphate, urine phosphate, plasma32P and32P specific activity (32P-S.A.) was studied using thyroparathyroidectomized rats. Radiophosphorus was injected at either 10 h (32P-10 h) or 8 days (32P-8 d) before commencing hormonal treatment. In order to produce consistent plasma32P-S.A. changes in rats treated with parathyroid hormone (PTH) alone, we maintained all animals for 48 h prior to hormone injection on a closely regulated carbohydrate intake (both quantity of food and time of feeding). Rats were then fasted 10 h prior to injection of PTH (0.01 U/g body weight/h), or CT (0.1 mU/g body weight/h), or both hormones injected simultaneously. Under these conditions, PTH produced a rise (relative to controls) in plasma32P-S.A. (-8 d) during an 8-h experimental period, while plasma32P-S.A. (-10 h) fell. Calcitonin treatment alone did not affect plasma32P-S.A., regardless of when32P was administered. When both hormones were injected concurrently, CT augmented the PTH-induced hypophosphatemia and magnified the fall in plasma32P levels, but the addition of CT did not affect PTH-induced changes in either renal calcium or phosphate excretion. However, the PTH-induced changes in plasma32P-S.A. were abolished. These data could not be explained by the opposing effects of the two hormones on rates of bone resorption. We interpret the results as adding support to the postulate that calcitonin moves phosphate into and prevents its loss from bone and bone fluid.

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