PTH is responsible for the maintenance of calcium homeostasis and normocalcemia. Secretion of PTH is stimulated or suppressed by perturbations in the serum calcium level. The calciotropic effects of PTH are mediated primarily by bone, where PTH-stimulated remodeling may release calcium to the extracellular fluid, and by the kidneys, where calcium reabsorption and phosphate excretion are increased. The effects of PTH in bone are bipolar: including regulation of multiple cell types, especially, both osteoblasts and osteoclasts, and stimulating both bone formation (anabolic effects) and bone resorption (catabolic) effects. The purpose of this review is to discuss the available data regarding PTH-regulated bone remodeling, the role of second messengers produced by polyphosphoinositide hydrolysis, the possible role of G proteins in regulating this reaction, and the biologic effects of activating this system. Greater insight into the complexities of parathyroid hormone-regulated bone remodeling are still required.

Original languageEnglish
Pages (from-to)38-42
Number of pages5
JournalContributions to Nephrology
StatePublished - 1991


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