Aquaporin-1 plays an essential role in water permeability and ultrafiltration during peritoneal dialysis
(2006) In Kidney International 69(9). p.1518-1525- Abstract
- The water channel aquaporin-1 (AQP1) is considered as the molecular counterpart of the ultrasmall pore predicted by the three-pore model of fluid transport across the peritoneal membrane. However, the definitive proof of the implication of AQP1 in solute-free water transport, sodium sieving, and ultrafiltration (UF) during peritoneal dialysis (PD) is lacking, and the effects of its deletion on the structure of the membrane are unknown. Using real-time reverse transcriptase-polymerase chain reaction and immunogold electron microscopy, we showed that AQP1 is the most abundant member of the AQP gene family expressed in the mouse peritoneum, and the only one located in the capillary endothelium. Transport studies during a 2-h dwell... (More)
- The water channel aquaporin-1 (AQP1) is considered as the molecular counterpart of the ultrasmall pore predicted by the three-pore model of fluid transport across the peritoneal membrane. However, the definitive proof of the implication of AQP1 in solute-free water transport, sodium sieving, and ultrafiltration (UF) during peritoneal dialysis (PD) is lacking, and the effects of its deletion on the structure of the membrane are unknown. Using real-time reverse transcriptase-polymerase chain reaction and immunogold electron microscopy, we showed that AQP1 is the most abundant member of the AQP gene family expressed in the mouse peritoneum, and the only one located in the capillary endothelium. Transport studies during a 2-h dwell demonstrated that, in comparison with Aqp1(+/+) littermates, Aqp1(-/-) mice had no sodium sieving; an B70% decrease in the initial, solute-free UF; and an B50% decrease in cumulative UF. These modifications occurred despite unchanged osmotic gradient and transport of small solutes in the Aqp1(-/-) mice. Heterozygous Aqp1(+/-) mice showed intermediate values in sodium sieving and initial UF, whereas cumulative UF was similar to Aqp1(+/+) mice. The deletion of AQP1 had no effect on the expression of other AQPs and on the density, structure, or diameter of peritoneal capillaries. These data provide direct evidence for the role of AQP1 during PD. They validate essential predictions of the three-pore model: (i) the ultrasmall pores account for the sodium sieving, and (ii) they mediate 50% of UF during a hypertonic dwell. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/410359
- author
- Ni, J ; Verbavatz, JM ; Rippe, Anna LU ; Boisde, I ; Moulin, P ; Rippe, Bengt LU ; Verkman, AS and Devuyst, O
- organization
- publishing date
- 2006
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- three-pore model, capillary endothelium, water channel, sodium sieving
- in
- Kidney International
- volume
- 69
- issue
- 9
- pages
- 1518 - 1525
- publisher
- Nature Publishing Group
- external identifiers
-
- wos:000237238400011
- pmid:16508653
- scopus:33646524077
- ISSN
- 1523-1755
- DOI
- 10.1038/sj.ki.5000285
- language
- English
- LU publication?
- yes
- id
- c1a4651c-7a34-437a-8efb-10a829dd73cb (old id 410359)
- date added to LUP
- 2016-04-01 17:00:40
- date last changed
- 2022-03-30 19:48:09
@article{c1a4651c-7a34-437a-8efb-10a829dd73cb,
abstract = {{The water channel aquaporin-1 (AQP1) is considered as the molecular counterpart of the ultrasmall pore predicted by the three-pore model of fluid transport across the peritoneal membrane. However, the definitive proof of the implication of AQP1 in solute-free water transport, sodium sieving, and ultrafiltration (UF) during peritoneal dialysis (PD) is lacking, and the effects of its deletion on the structure of the membrane are unknown. Using real-time reverse transcriptase-polymerase chain reaction and immunogold electron microscopy, we showed that AQP1 is the most abundant member of the AQP gene family expressed in the mouse peritoneum, and the only one located in the capillary endothelium. Transport studies during a 2-h dwell demonstrated that, in comparison with Aqp1(+/+) littermates, Aqp1(-/-) mice had no sodium sieving; an B70% decrease in the initial, solute-free UF; and an B50% decrease in cumulative UF. These modifications occurred despite unchanged osmotic gradient and transport of small solutes in the Aqp1(-/-) mice. Heterozygous Aqp1(+/-) mice showed intermediate values in sodium sieving and initial UF, whereas cumulative UF was similar to Aqp1(+/+) mice. The deletion of AQP1 had no effect on the expression of other AQPs and on the density, structure, or diameter of peritoneal capillaries. These data provide direct evidence for the role of AQP1 during PD. They validate essential predictions of the three-pore model: (i) the ultrasmall pores account for the sodium sieving, and (ii) they mediate 50% of UF during a hypertonic dwell.}},
author = {{Ni, J and Verbavatz, JM and Rippe, Anna and Boisde, I and Moulin, P and Rippe, Bengt and Verkman, AS and Devuyst, O}},
issn = {{1523-1755}},
keywords = {{three-pore model; capillary endothelium; water channel; sodium sieving}},
language = {{eng}},
number = {{9}},
pages = {{1518--1525}},
publisher = {{Nature Publishing Group}},
series = {{Kidney International}},
title = {{Aquaporin-1 plays an essential role in water permeability and ultrafiltration during peritoneal dialysis}},
url = {{http://dx.doi.org/10.1038/sj.ki.5000285}},
doi = {{10.1038/sj.ki.5000285}},
volume = {{69}},
year = {{2006}},
}