Water transport across the peritoneal membrane
(2014) In Kidney International 85(4). p.750-758- Abstract
- Peritoneal dialysis involves diffusive and convective transports and osmosis through the highly vascularized peritoneal membrane. The capillary endothelium offers the rate-limiting hindrance for solute and water transport. It can be functionally described in terms of a three-pore model including transcellular, ultrasmall pores responsible for free-water transport during crystalloid osmosis. Several lines of evidence have demonstrated that the water channel aquaporin-1 (AQP1) corresponds to the ultrasmall pore located in endothelial cells. Studies in Aqp1 mice have shown that deletion of AQP1 is reflected by a 50% decrease in ultrafiltration and a disappearance of the sodium sieving. Haploinsufficiency in AQP1 is also reflected by a... (More)
- Peritoneal dialysis involves diffusive and convective transports and osmosis through the highly vascularized peritoneal membrane. The capillary endothelium offers the rate-limiting hindrance for solute and water transport. It can be functionally described in terms of a three-pore model including transcellular, ultrasmall pores responsible for free-water transport during crystalloid osmosis. Several lines of evidence have demonstrated that the water channel aquaporin-1 (AQP1) corresponds to the ultrasmall pore located in endothelial cells. Studies in Aqp1 mice have shown that deletion of AQP1 is reflected by a 50% decrease in ultrafiltration and a disappearance of the sodium sieving. Haploinsufficiency in AQP1 is also reflected by a significant attenuation of water transport. Conversely, studies in a rat model and in PD patients have shown that the induction of AQP1 in peritoneal capillaries by corticosteroids is reflected by increased water transport and ultrafiltration, without affecting the osmotic gradient and small-solute transport. Recent data have demonstrated that a novel agonist of AQP1, predicted to stabilize the open-state conformation of the channel, modulates water transport and improves ultrafiltration. Whether increasing the expression of AQP1 or gating the already existing channels would be clinically useful in PD patients remains to be investigated. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4439635
- author
- Devuyst, Olivier and Rippe, Bengt LU
- organization
- publishing date
- 2014
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- endothelial cells, peritoneal dialysis, water channels
- in
- Kidney International
- volume
- 85
- issue
- 4
- pages
- 750 - 758
- publisher
- Nature Publishing Group
- external identifiers
-
- wos:000333746200010
- scopus:84897954248
- pmid:23802191
- ISSN
- 1523-1755
- DOI
- 10.1038/ki.2013.250
- language
- English
- LU publication?
- yes
- id
- 851250e7-3cc2-491f-a09a-4ad66898c584 (old id 4439635)
- date added to LUP
- 2016-04-01 13:47:50
- date last changed
- 2022-04-06 07:06:25
@article{851250e7-3cc2-491f-a09a-4ad66898c584,
abstract = {{Peritoneal dialysis involves diffusive and convective transports and osmosis through the highly vascularized peritoneal membrane. The capillary endothelium offers the rate-limiting hindrance for solute and water transport. It can be functionally described in terms of a three-pore model including transcellular, ultrasmall pores responsible for free-water transport during crystalloid osmosis. Several lines of evidence have demonstrated that the water channel aquaporin-1 (AQP1) corresponds to the ultrasmall pore located in endothelial cells. Studies in Aqp1 mice have shown that deletion of AQP1 is reflected by a 50% decrease in ultrafiltration and a disappearance of the sodium sieving. Haploinsufficiency in AQP1 is also reflected by a significant attenuation of water transport. Conversely, studies in a rat model and in PD patients have shown that the induction of AQP1 in peritoneal capillaries by corticosteroids is reflected by increased water transport and ultrafiltration, without affecting the osmotic gradient and small-solute transport. Recent data have demonstrated that a novel agonist of AQP1, predicted to stabilize the open-state conformation of the channel, modulates water transport and improves ultrafiltration. Whether increasing the expression of AQP1 or gating the already existing channels would be clinically useful in PD patients remains to be investigated.}},
author = {{Devuyst, Olivier and Rippe, Bengt}},
issn = {{1523-1755}},
keywords = {{endothelial cells; peritoneal dialysis; water channels}},
language = {{eng}},
number = {{4}},
pages = {{750--758}},
publisher = {{Nature Publishing Group}},
series = {{Kidney International}},
title = {{Water transport across the peritoneal membrane}},
url = {{http://dx.doi.org/10.1038/ki.2013.250}},
doi = {{10.1038/ki.2013.250}},
volume = {{85}},
year = {{2014}},
}