NDT Advance Access published online on May 3, 2007
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm214
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Does kidney amino acid transport have something to do with blood pressure?*
Institute of Physiology and Centre for Integrative Human Physiology (ZIHP), University of Zürich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland
Correspondence and offprint requests to: François Verrey, Institute of Physiology, University of Zürich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland. Email: verrey@access.uzh.ch
Keywords: Amino acid transport; Angiotensin-converting enzyme; B0AT1; Blood pressure; cotransporter; kidney proximal tubule; SLC6A19; TMEM27
| The first 150 words of the full text of this article appear below. |
A paper recently published in Nature by Danilczyk et al. shows that collectrin (Tmem27), a homologue of angiotensin-converting enzyme 2 (ACE2), surprisingly plays a central role in kidney amino acid transport [1]. This was discovered when the phenotype of a collectrin knock out mouse, generated in the laboratory of Josef Penninger, was analysed. The deficiency of this relatively short type I transmembrane protein causes a massive urinary loss of neutral amino acids (NAA) that even leads to the formation of urinary amino acid crystals. This was shown to be the consequence of a major impairment of amino acid reabsorption, due to the fact that collectrin is necessary for the functional expression of major Na+amino acid cotransporters of kidney proximal tubule. The analysis of another collectrin knock out mouse, published in the American Journal of Physiology: Renal Physiology by Malakauskas et al. [2],
| Amino acid reabsorption in proximal kidney tubule |
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| The SLC6 Na+amino acid cotransporters of the kidney |
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| Comparison with heteromeric amino acid transporters and open questions |
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