Parathyroid hormone (PTH) is the key endocrine factor regulating systemic Ca2+ homeostasis. Elevated levels of circulating PTH increase bone turnover and, depending on the duration of elevation, will result in net anabolic or catabolic effects on the skeleton. Secretion of PTH from the parathyroid glands is regulated by small changes in circulating levels of Ca2+ which are detected by a Ca2+ receptor on the surface of parathyroid cells. This G protein-coupled receptor is the primary molecular entity used by parathyroid cells to regulate secretion of PTH. As such, the Ca2+ receptor is a unique molecular target for new drugs capable of increasing or decreasing circulating levels of PTH. Compounds which activate the Ca2+ receptor are termed calcimimetics and they inhibit the secretion of PTH, a calcimimetic compound is in late stage clinical trials for the treatment of both primary and secondary hyperparathyroidism. Conversely, calcilytic compounds, which are Ca2+ receptor antagonists, stimulate secreti on of PTH, a calcilytic compound is in early clinical development for the treatment of osteoporosis.
Keywords: Pharmacological Regulation, Parathyroid Hormone, Calcimimetics, Calcilytics, HYPERPARATHYROIDISM, Osteodystrophy
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