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Nephrol Dial Transplant (2003) 18: 2467-2470
© 2003 European Renal Association-European Dialysis and Transplant Association

Editorial Comment

Calcium-sensing receptor and renal cation handling

Pascal Houillier and Michel Paillard

Département de Physiologie, Hôpital Européen Georges Pompidou, Assistance Publique – Hôpitaux de Paris, Université Pierre et Marie Curie, INSERM U356, Institut Fédératif de Recherche 58, Paris, France.

Correspondence and offprint requests to: Pascal Houillier, MD, PhD, Département de Physiologie, Hôpital Européen Georges Pompidou, 20 rue Leblanc, F-75015 Paris, France. Email: pascal.houillier@egp.ap-hop-paris.fr

Keywords: calcium-sensing receptor; cortical thick ascending limb; renal tubular cation handling

The first 150 words of the full text of this article appear below.



   Introduction
 
Renal tubular calcium reabsorption is a critical determinant of extracellular fluid (ECF) calcium concentration; for the need of constancy of ECF calcium concentration, the renal tubular handling of calcium is tightly controlled in order to match renal calcium excretion to the net amount of calcium entering the ECF. Both parathyroid hormone (PTH) and vitamin D metabolites are involved in the control of renal tubular calcium reabsorption and ECF calcium concentration [1]. Besides this hormonal control, it has been recognized recently that ECF calcium is able to regulate its own reabsorption by the mammalian tubule. Indeed, a large body of evidence supports the view that ECF calcium exerts this action by activating the calcium/polyvalent cation-sensing receptor (CaSR) located in the plasma membrane of many tubular cell types. First, increasing ECF calcium concentration elicits a marked increase in urinary calcium (and magnesium) excretion [2,3] and this . . . [Full Text of this Article]



   Localization of the extracellular CaSR
 


   CaSR under physiological conditions
 


   CaSR under pathological conditions
 

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