Abstract
Chronically parathyroidectomized rats counteracted the hypercalcemia induced by intraperitoneal injection of calcium more rapidly than thyroparathyroidectomized rats, whether the rats compared were thyroxinetreated or not. The results indicate that the thyroid alone, in the absence of all parathyroid secretions, effects a calcium-lowering response in hypercalcemia in the rat, presumably by the release of thyrocalcitonin, a polypeptide with demonstrated calcium-lowering activity. The thyroxine-dependent metabolic status of the animals also played a part in the rate of elimination of an exogenous hypercalcemia. The elimination was more rapid in thyroxine-treated than in saline-treated rats, whether normal thyroid tissue was present or not. Hence, evaluation of calcium tolerance after thyroidectomy requires consideration of the additive effects of lack of thyrocalcitonin and incipient classic hypothyroidism. (Endocrinology 79: 1033, 1966)
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