To investigate the relation between the hypocalcemic activity of thyrocalci-tonin and the rate of bone resorption, the quantitative effect of exogenous thyrocalcitonin was studied in rats in which the rate of bone resorption was altered by thyroparathyroidectomy and by the administi’ation of calcium salts, parathyroid extract or vitamin D3. In sham-operated rats made hypercalcemic by the oral administration of CaCl2, thyrocalcitonin had no significant hypocalcemic activity. In thyroparathyroidec-tomized rats given oral CaCl2, a full Hypocalcemic response to thyrocalcitonin, of 1.49 mEq/I, occurred. In sham-operated and thyropara thyroid-ectomized rats made hypercalcemic by the administration of parathyroid extract, thyrocalcitonin caused mean decreases in the plasma concentration of calcium of 0.83 and 1.47 mEq/I, respectively. In hypercalcemia produced by the administration of a single dose of 105USP U of vitamin D3, sham-operated and thyroparathyroidectomized rats showed mean decreases in the plasma concentration of calcium of 1.32 and 1.24 mEq/I, respectively, during thyrocalcitonin administration. A similar hypocalcemic response was seen in thyroparathyroidectomized rats given a 10-fold greater dose of vitamin D3. In collateral studies of the release of 86Sr from the skeleton, thyroparathyroidectomy decreased, and vitamin D3administration markedly increased, the ratio of urinary85Sr to tibial85Sr. The administration of thyrocalcitonin produced decreases in the excretion of85Sr which were parallel to the control values for the ratio of urinary85Sr to tibial85Sr. These data indicate that the degree to which thyrocalcitonin can inhibit bone resorption is dependent upon the prevailing rate of bone resorption. This characteristic of thyrocalcitonin action may be significant in the treatment of human hypercalcemia with thyrocalcitonin.
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