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Nephrol Dial Transplant (2004) 19: v20-v26
Nephrol Dial Transplant Vol. 19 Suppl 5 © ERA–EDTA 2004; all rights reserved

Modulation and action of the calcium-sensing receptor

Tilman B. Drüeke

INSERM Unit 507 and Service de Néphrologie, Hôpital Necker, Paris, France

Correspondence and offprint requests to: Professor Tilman B. Drüeke, INSERM Unit 507 and Service de Néphrologie, Hôpital Necker, Paris, France. Email: drueke{at}necker.fr

Abstract

The discovery and cloning of the calcium-sensing receptor (CaR) in 1993 has led to a better understanding of the regulation of calcium homoeostasis. Following activation by extracellular calcium ions, the CaR triggers a cascade of intracellular events. These events result in the release of secondary messengers, which have a number of biological effects, the most important of which is a reduction in parathyroid hormone (PTH) secretion. The way in which calcium acts on the CaR varies depending on the cell type. In the parathyroid gland cell, activation of the CaR by elevated serum levels of calcium leads to a decrease in PTH secretion. In the kidney, CaR activation is thought to have several different actions, leading to enhanced reabsorption of sodium chloride and increased calcium and magnesium excretion in the renal tubules. CaRs are also found in other tissues in the body that are not involved in calcium homoeostasis, suggesting that the CaR has actions that are not associated with calcium homoeostasis. In patients with end-stage renal disease, parathyroid gland hyperplasia is associated with downregulation of the CaR. Discovery of the CaR has allowed the development of a group of drugs called calcimimetics, which mimic or potentiate the actions of extracellular calcium on the CaR. These compounds have considerable potential for the treatment of primary and secondary hyperparathyroidism.

Keywords: calcimimetics; calcium-sensing receptor; parathyroid gland; parathyroid hormone; secondary hyperparathyroidism


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