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Active Ca(2+) reabsorption in the connecting tubule
Sandor Boros1, René J M Bindels, Joost G J Hoenderop
1Department of Physiology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, The Netherlands.
Pflugers Archiv : European Journal of Physiology
|November 8, 2008
Summary
The kidney reabsorbs calcium (Ca2+) in the distal tubules using the TRPV5 channel. New mechanisms involving klotho and tissue kallikrein offer potential treatments for renal calcium wasting.
Area of Science:
- Nephrology
- Molecular Biology
- Physiology
Background:
- The kidney is vital for maintaining the body's calcium (Ca2+) balance.
- Active Ca2+ reabsorption occurs in the distal convoluted tubules (DCT2) and connecting tubules (CNT) of the nephron.
- This process is primarily mediated by the transient receptor potential vanilloid 5 (TRPV5) epithelial Ca2+ channel.
Purpose of the Study:
- To review the molecular mechanisms of active Ca2+ reabsorption in the kidney.
- To highlight the roles of hormones and novel regulatory factors in Ca2+ transport.
- To identify potential pharmacological targets for treating renal Ca2+ wasting.
Main Methods:
- Literature review of studies on renal Ca2+ handling.
- Analysis of molecular pathways involved in Ca2+ transport.
- Discussion of regulatory mechanisms of TRPV5 channel activity.
Main Results:
- Active Ca2+ reabsorption involves apical entry, cytoplasmic transport, and basolateral extrusion.
- Hormones like 1,25-dihydroxyvitamin D3, parathyroid hormone, and estrogen regulate Ca2+ transport.
- Klotho and tissue kallikrein directly influence TRPV5 channel abundance at the apical membrane.
Conclusions:
- Understanding the molecular steps of Ca2+ reabsorption is crucial for kidney function.
- Novel regulatory mechanisms, including klotho and tissue kallikrein, offer new therapeutic avenues.
- Targeting these mechanisms could lead to effective treatments for renal Ca2+ wasting disorders.
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