Calcitonin—a Hormone from the Parathyroid which Lowers the Calcium-level of the Blood

@article{Copp1962CalcitoninaHF,
  title={Calcitonin—a Hormone from the Parathyroid which Lowers the Calcium-level of the Blood},
  author={D. Harold Copp and B A Cheney},
  journal={Nature},
  year={1962},
  volume={193},
  pages={381-382}
}
CONTROL of the calcium-level in blood is the primary function of the parathyroids. McLean1 has suggested that this is accomplished through a ‘feedback’ mechanism, by which a low level of calcium in the blood stimulates the glands to produce parathyroid hormone which in turn mobilizes calcium from bone and restores the normal level. High levels of calcium are assumed to suppress production of this hormone. 
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Calcitonin was discovered more than 40 years ago as a hormone that lowers circulating calcium levels [14, 15]. In mammals, the major site of calcitonin synthesis is the parafollicular cells of the
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References

SHOWING 1-2 OF 2 REFERENCES
Direct Humoral Control of Parathyroid Function in the Dog.∗ †
  • D. Copp, A. Davidson
  • Biology, Medicine
    Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine
  • 1961
TLDR
A “feedback” mechanism involving the parathyroids which is sufficiently sensitive and fast-acting to account for the acute homeostatic control of blood calcium is indicated.
THE PARATHYROIDS—PHYSIOLOGY AND THERAPEUTICS
TLDR
The parathyroid hormone apparently regulates the level of calcium ions, and there is considerable circumstantial evidence that the stimulus is phosphorus metabolism, which is dependent on the preceding changes in the metabolism of phosphorus.