THYROCALCITONIN AND ITS ROLE IN CALCIUM HOMEOSTASIS

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Abstract
SUMMARY: In pigs, the control of hypercalcaemia was significantly impaired by thyroidectomy. Hypercalcaemic perfusion of the pig thyroid (which contains no parathyroids) in situ produced a systemic hypocalcaemic response which reached its maximum after about 2 hr. perfusion and which persisted for as long as the hypercalcaemic stimulus was applied. Thyroid venous plasma from a gland so perfused, when cross-transfused into a second pig, caused a hypocalcaemic reaction similar to that produced by the intravenous injection of porcine thyrocalcitonin preparations. Hypermagnesaemia did not appear to influence the release of thyrocalcitonin. A hypocalcaemic response to hypercalcaemic perfusion of the thyroid, similar to that seen in intact pigs, occurred in parathyroidectomized pigs, provided that the initial plasma calcium level was maintained by suitable calcium supplement to the diet. Hypocalcaemic perfusion of the thyroid, in either intact or parathyroidectomized pigs, resulted in a rise in the systemic plasma calcium concentration, although this rise was only consistently observed when the systemic plasma calcium level was already low as a result of thyrocalcitonin secretion. It is suggested that the secretion of thyrocalcitonin is controlled by a negative feedback mechanism operating through the plasma calcium concentration, and that because of the rapidity of its release, action and elimination, relative to parathyroid hormone, thyrocalcitonin acts as a fine regulator of calcium homeostasis.