Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-2-8
pubmed:abstractText
Aquaporin (AQP) water channel AQP3 has been proposed to be the major glycerol and non-AQP1 water transporter in erythrocytes. AQP1 and AQP3 are also expressed in the kidney where their deletion in mice produces distinct forms of nephrogenic diabetes insipidus. Here AQP1/AQP3 double knockout mice were generated and analyzed to investigate the functional role of AQP3 in erythrocytes and kidneys. 53 double knockout mice were born out of 756 pups from breeding double heterozygous mice. The double knockout mice had reduced survival and impaired growth compared with the single knockout mice. Erythrocyte water permeability was 7-fold reduced by AQP1 deletion but not further reduced in AQP1/AQP3 null mice. AQP3 deletion did not affect erythrocyte glycerol permeability or its inhibition by phloretin. Daily urine output in AQP1/AQP3 double knockout mice (15 ml) was 9-fold greater than in wild-type mice, and urine osmolality (194 mosm) was 8.4-fold reduced. The mice remained polyuric after DDAVP administration or water deprivation. The renal medulla in most AQP1/AQP3 null mice by age 4 weeks was atrophic and fluid-filled due to the severe polyuria and hydronephrosis. Our data provide direct evidence that AQP3 is not functionally important in erythrocyte water or glycerol permeability. The renal function studies indicate independent roles of AQP1 and AQP3 in countercurrent exchange and collecting duct osmotic equilibration, respectively.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
276
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
624-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11035042-Animals, pubmed-meshheading:11035042-Aquaporin 1, pubmed-meshheading:11035042-Aquaporin 3, pubmed-meshheading:11035042-Aquaporins, pubmed-meshheading:11035042-Cell Membrane Permeability, pubmed-meshheading:11035042-Cell Size, pubmed-meshheading:11035042-Diabetes Insipidus, Nephrogenic, pubmed-meshheading:11035042-Erythrocytes, pubmed-meshheading:11035042-Fluorescent Antibody Technique, pubmed-meshheading:11035042-Gene Deletion, pubmed-meshheading:11035042-Glycerol, pubmed-meshheading:11035042-Hydronephrosis, pubmed-meshheading:11035042-Kidney, pubmed-meshheading:11035042-Kidney Concentrating Ability, pubmed-meshheading:11035042-Kidney Function Tests, pubmed-meshheading:11035042-Kidney Tubules, Collecting, pubmed-meshheading:11035042-Mercuric Chloride, pubmed-meshheading:11035042-Mice, pubmed-meshheading:11035042-Mice, Knockout, pubmed-meshheading:11035042-Osmolar Concentration, pubmed-meshheading:11035042-Survival Rate, pubmed-meshheading:11035042-Urine, pubmed-meshheading:11035042-Water
pubmed:year
2001
pubmed:articleTitle
Erythrocyte water permeability and renal function in double knockout mice lacking aquaporin-1 and aquaporin-3.
pubmed:affiliation
Department of Medicine, Cardiovascular Research Institute, University of California, San Francisco, California, 94143-0521, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't