discussed earlier, inhibition of osteoclastic activity by calcitonin eventually decreases osteoblastic activity as well. All cell types appear quiescent in histological sections of bone that were chronically exposed to high concentrations of calcitonin. Although osteoclasts express very high numbers of receptors for calcitonin, they quickly become insensitive to the hormone because continued stimulation results in massive down-regulation of the receptors.
At high concentrations calcitonin may increase urinary excretion of calcium and phosphorus, probably by acting on the proximal tubules. In humans these effects are small, last only a short while, and are not physiologically important for lowering blood calcium. Renal handling of calcium is not disrupted in patients with thyroid tumors that secrete large amounts of calcitonin. Kidney cells "escape" from prolonged stimulation with calcitonin and become refractory to it, probably as a result of down-regulation of receptors.
Circulating concentrations of calcitonin are low when blood calcium is in the normal range or below, but they increase proportionately when calcium rises above about 9 mg/dL (Fig. 14). Parafollicular cells respond directly to ionized calcium in blood and express the same G-protein-coupled calcium sensing receptor in their surface membranes as the parathyroid chief cells. Both cell types respond to extracellular calcium over the ecc o i i—
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