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Bas et al. (1), in this issue, have demonstrated that acute hypercalcemic clamp over 2 h in rabbits reduces the subsequent intact (I) parathyroid hormone (PTH) response to hypocalcemia by 50%, while chronic hyper- calcemia, secondary to experimental renal failure in the same animal model, fails to reduce the I-PTH response to hypocalcemia. These results raise questions about the acute and chronic influence of calcium concen- tration on parathyroid function and on circulating PTH molecular forms. To understand and appropriately discuss these differences, it is necessary to review various aspects of PTH physiology. Circulating PTH is immunoheterogenous. Under normocalcemic conditions, it is composed of 20% PTH(1 - 84), the biologically active form of the hor- mone on the PTH/PTHrP receptor, and of 80% carboxyl- terminal (C) fragments, considered until recently to be biologically inactive (2, 3). The main circulating C-PTH fragments observed during the peripheral

Effects of acute and chronic hypercalcemia on parathyroid function and circulating parathyroid hormone molecular forms