It has been previously observed that perfusion of the thyroid-parathyroid gland complex in the dog with high calcium blood results in liberation of a hypocalcemic factor, calcitonin. In sheep, the superior parathyroid gland is separated by 2–3 cm from the thyroid and has a distinct blood supply, so that it can be perfused independently. Perfusion of this gland with high calcium blood (10.8–12.8 mg/100 ml) in 6 sheep, 3 of which had been thyroidectomized immediately prior to perfusion, resulted in a prompt fall in systemic plasma calcium, the change in 30 min being -0.530 ±0.074 mg/100 ml. Subsequently, in 5 adult sheep and 5 lambs, the thyroid was first perfused with high calcium blood for 1 hr, and then the superior parathyroid. Perfusion of the thyroid had no significant effect on systemic plasma calcium, but perfusion of the superior parathyroid resulted in a significant fall at 10 min and a change of -0.706 ±0.088 mg/100 ml by 30 min. The drop 30 min following parathyroidectomy was small and not statistically significant. It was concluded that the parathyroid rather than thyroid was the source of the hypocalcemic hormone, calcitonin, released by the stimulus of hypercalcemia. (Endocrinology75: 49, 1964)
No takes yet. Share an insight, caveat, or question.
Copp et al. (1964) studied this question.
Synapse has enriched one closely related paper. Consider it for comparative context: