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Pflugers Arch. 2005 Oct;451(1):181-92. Epub 2005 Jul 26.

TRPV5 and TRPV6 in Ca(2+) (re)absorption: regulating Ca(2+) entry at the gate.

Author information

1
Department of Physiology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands.

Abstract

Many physiological functions rely on the exact maintenance of body Ca(2+) balance. Therefore, the extracellular Ca(2+) concentration is tightly regulated by the concerted actions of intestinal Ca(2+) absorption, exchange of Ca(2+) to and from bone, and renal Ca(2+) reabsorption. Renal distal convoluted and connecting tubular cells as well as duodenal epithelial cells are unique in their ability to mediate transcellular (re)absorption of Ca(2+) at large and highly variable rates. Two members of the transient receptor potential (TRP) superfamily, TRP vanilloid (TRPV)5 and TRPV6, are specialized epithelial Ca(2+) channels responsible for the critical Ca(2+) entry step in transcellular Ca(2+) (re)absorption in intestine and kidney, respectively. Because transcellular Ca(2+) transport is fine-tuned to the body's specific requirements, regulation of the transmembrane Ca(2+) flux through TRPV5/6 is of particular importance and has, therefore, to be conspicuously controlled. We present an overview of the current knowledge and recent advances concerning the coordinated regulation of Ca(2+) influx through the epithelial Ca(2+) channels TRPV5 and TRPV6 in transcellular Ca(2+) (re)absorption.

PMID:
16044309
DOI:
10.1007/s00424-005-1430-6
[Indexed for MEDLINE]

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