Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

The cloning of the BoPCaR1 gene has helped to elucidate many aspects of normal extracellular calcium homeostasis, particularly as applied to the regulation of PTH secretion, calcitonin secretion and renal calcium reabsorption. In addition, loss and gain of function mutations have been found to cause the clinical syndromes of FBH, NSHPT and ADHH respectively. The CaR has also been implicated in the mechanisms leading to primary and uraemic hyperparathyroidism, and autoimmune parathyroid destruction. The recent demonstration that the CaR regulates non-selective cation channel function in rat hippocampal neurones suggests that it may also have a role within the central nervous system that is entirely unrelated to calcium homeostasis (Ye et al. 1996). Finally, the prospect of CaR agonists and antagonists, which may allow PTH secretion to be regulated independently of the serum calcium concentration, also holds much promise for the medical treatment of hyperparathyroidism, renal osteodystrophy and osteoporosis.

Type

Journal article

Journal

J Endocrinol

Publication Date

09/1997

Volume

154

Pages

371 - 378

Keywords

Calcium, Extracellular Space, Homeostasis, Humans, Parathyroid Diseases, Parathyroid Glands, Receptors, Calcium-Sensing, Receptors, Cell Surface