Abstract
The cloning of the CaR has made it possible to show definitively that the CaR is a critical mediator of the inhibitory effect of high Cao2+ on PTH secretion and parathyroid cellular proliferation. The receptor may also mediate the suppressive action of high Cao2+ on PTH gene expression, while its involvement in several other known actions of Cao2+ on parathyroid function remain to be examined. Alterations in CaR expression and/or function are clearly involved in hyper- and hypocalcemic disorders caused by inactivating or activating CaR mutations, respectively, and could contribute to the deranged Cao(2+)-sensing in primary and uremic secondary HPT. Finally, CaR activators offer promise as the first truly effective mode of medical therapy for these latter two conditions.
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