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Abstract
It has long been recognized that the secretion of PTH by chief cells in the parathyroid gland is regulated by extracellular ionized calcium. The molecular mechanism by which extracellular Ca2+ performs this feat was deduced by the cloning of the extracellular calcium-sensing receptor (CaSR) in 1993 in the laboratories of Brown and Hebert. The CaSR is a G protein-coupled cell surface receptor that belongs to family 3 of the GPCR superfamily. The CaSR senses the extracellular ionic activity of the divalent minerals Ca2+ and Mg2+ and translates this information, via a complex array of cellular signaling pathways, to modify cell and tissue function. Genetic studies have demonstrated that the activity of this receptor determines the steady-state plasma calcium concentration in humans by regulating key elements in the calcium homeostatic system. CaSR agonists (calcimimetics) and antagonists (calcilytics) have been identified and have provided both current and potential therapies for a variety of disorders. Calcimimetics can effectively reduce PTH secretion in all forms of hyperparathyroidism. They are likely to become a major therapy for secondary hyperparathyroidism associated with renal failure and for treatment of certain patients with primary hyperparathyroidism. On the therapeutic horizon are calcilytics that can transiently increase PTH and may prove useful in the treatment of osteoporosis.
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