Abstract

1. 1. Net calcium absorption from the gut, S i , can be considered the input that disturbs plasma Ca which in turn is regulated by the net calcium balance of bone, Δ, and urinary calcium excretion, v u . A comparison of the plasma calcium level as a function of S i in thyroidectomized (TX) and control (C) animals, both groups bearing parathyroid autografts and supplied with three levels of calcium intake, the TX animals receiving l-thyroxin, failed to reveal differences in either their capacity for or intensity of plasma calcium regulation. 2. 2. Net calcium balance in bone is the difference between calcium deposition in bone, v 0 + , and removal from bone, v 0 − . Lack of endogenous thyrocalcitonin failed to affect the intensity of v 0 + or v 0 − or the relationships between S i and v 0 + or v 0 − . Hence, thyrocalcitonin has no effect on the relative or absolute importance of v 0 + and v 0 − in regulation. Moreover, there were no differences in bone calcium between C and TX animals. 3. 3. Lack of endogenous thyrocalcitonin also had no effect on urinary calcium excretion nor on the relative importance of the kidney in regulating plasma calcium. Thus the lack of thyrocalcitonin can be seen to have had no steady state effect on the calcium metabolism of the rat and it is unlikely that this hormone plays a steady state role. 4. 4. Similar detailed comparisons of control (C) animals with normal intact (N) rats revealed differences which, though small, were often of greater magnitude than the differences between C and TX animals. The differences between C and N animals were of the type and direction observed in a comparable study of N and parathyroidectomized rats. The differences between C and N animals thus point to the profound steady state role played by parathyroid hormone in the regulation of calcium metabolism and further indicate why the nature of the control exerted by thyrocalcitonin cannot be comparable to that exerted by parathyroid hormone.

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