Abstract
The calcium-sensing receptor represents the molecular mechanism by which parathyroid chief cells detect changes in plasma ionized calcium concentration and modulate parathyroid hormone secretion to maintain serum calcium levels within a narrow physiological range. Beyond this classic role signaling through the calcium-sensing receptor also influence both PTH gene transcription and cell proliferating of the parathyroid cells.
The other role calcium-sensing receptor plays in the tubular system of the kidney, where it regulates calcium excretion. Mutations within the gene for calcium-sensing receptor result in gain or loss of receptor function.
Inactivating mutations are in heterozygous form associated to familiar benign hypocalciuric hypercalcemia and in homozygous form to neonatal severe primary hyperparathyroidism. Activating mutations are associated to autotosomal dominant hypocalcemia with hypercalciuria and Bartter's syndrome type V.
The new use plays its allosteric modulators that modify its function with therapeutic applications in patients suffered from parathyroid gland dysfunction.