Homeostasis of Plasma Calcium: Effects of Actinomycin D, Parathyroidectomy and Thyrocalcitonin

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Abstract
One hr. after subcutaneous administration of thyrocalcitonin (5-10 U) to intact rats the plasma calcium concentration reached its lowest leve. The same acute hypocalcemic effect was observed in rats that had been given actinomycin D or that were parathyroidectomized by surgical excision. Plasma calcium concentration returned to normal in control rats between 1 and 3 hr after thyrocalcitonin. However, there was no rise in plasma calcium during this same 2-hr interval in rats injected with actinomycin D 7 hr previously or in rats surgically parathyroidectomized at the time they were injected with thyrocalcitonin. Actinomycin-treated rats that did not receive thyrocalcitonin maintained normal plasma calcium concentrations for 12 hr. Thereafter, the plasma calcium level of rats treated with actinomycin D alone fell at a rate similar to the rate of fall after parathyroidectomy by surgical excision. The parathyroid glands from hypocalcemic. actinomycintreated rats were homotransplanted to parathyroidectomized recipient rats. The transplanted glands from actinomycintreated rats maintained the same plasma calcium level in recipient rats as glands from control donors. These data demonstrate that in the actinomycin-treated rat the parathyroid gland cannot maintain a normal plasma calcium concentration, and they show that parathyroid hormone synthesis is not inhibited, or if it is, the inhibition is reversible. It is concluded that the short duration of the hypocalcemic effect of thyrocalcitonin in intact rats is due, at least in part, to the activity of the parathyroid gland, presumably to the calcium-mobilizing action of parathyroid hormone.