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Disorders of calcium ion sensing.

T HE PARATHYROID glands secrete parathyroid hormone (PTH) at a rate that is dependent upon and responsive to the extracellular calcium ion concentration (Ca*‘,) (1). Recent advances in molecular techniques have enabled the characterization of an extracellular calcium ionsensing receptor (Can) that initiates the afferent limb of the cellular pathways necessary for regulating this Ca2’0-responsive PTH secretion (2). Renal tubular calcium reabsorption, secretion of calcitonin by the thyroidal C-cells, and probably many other Ca2t0responsive cellular functions are dependent upon the CaR to permit the regulation of extracellular calcium homeostasis and other diverse cellular functions unrelated to calcium homeostasis, such as found in the brain. We will review the biochemical and molecular characteristics of the CaR as well as three disorders: familial benign hypocalciuric hypercalcemia, neonatal severe hyperparathyroidism, and autosomal dominant hypocalcemia, which are caused by abnormalities of CaR function (3, 4).