| http://purl.uniprot.org/citations/11133517 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/11133517 | http://www.w3.org/2000/01/rdf-schema#comment | "The CLC-K1 chloride channel is a kidney-specific CLC chloride channel expressed in the thin ascending limb of Henle's loop (tAL). Recently, we determined that Clcnk1-/-mice show nephrogenic diabetes insipidus (NDI). To investigate the pathogenesis of impaired urinary concentrating ability, we analyzed renal functions of Clcnk1-/-mice in more detail. The osmolar clearance-to-creatinine clearance ratio was not significantly different between Clcnk1+/- and Clcnk1+/+ mice. Fractional excretion of sodium, chloride, and urea was also not significantly affected in Clcnk1-/-mice. These results indicate that the polyuria observed in Clcnk1-/-mice was water diuresis and not osmotic diuresis. The papillary osmolarity in Clcnk1-/-mice was significantly lower than that in Clcnk1+/+ mice under a hydrated condition, and it did not increase even after water deprivation. Sodium and chloride contents in the inner medulla in Clcnk1-/-mice were at about one-half the levels observed in Clcnk1+/+ mice. Furthermore, the accumulation of urea was also impaired in Clcnk1-/-mice, suggesting that the overall countercurrent system was impaired by a defect of its single component, chloride transport in the tAL. The aldose reductase mRNA abundance in Clcnk1-/-mice was decreased, further evincing that inner medullary tonicity is decreased in Clcnk1-/- mice. We concluded that NDI in Clcnk1-/-mice resulted from an impairment in the generation of inner medullary hypertonicity by a dysfunction of the countercurrent systems."xsd:string |
| http://purl.uniprot.org/citations/11133517 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajprenal.2001.280.1.f79"xsd:string |
| http://purl.uniprot.org/citations/11133517 | http://purl.uniprot.org/core/author | "Sasaki S."xsd:string |
| http://purl.uniprot.org/citations/11133517 | http://purl.uniprot.org/core/author | "Marumo F."xsd:string |
| http://purl.uniprot.org/citations/11133517 | http://purl.uniprot.org/core/author | "Uchida S."xsd:string |
| http://purl.uniprot.org/citations/11133517 | http://purl.uniprot.org/core/author | "Akizuki N."xsd:string |
| http://purl.uniprot.org/citations/11133517 | http://purl.uniprot.org/core/date | "2001"xsd:gYear |
| http://purl.uniprot.org/citations/11133517 | http://purl.uniprot.org/core/name | "Am J Physiol Renal Physiol"xsd:string |
| http://purl.uniprot.org/citations/11133517 | http://purl.uniprot.org/core/pages | "F79-87"xsd:string |
| http://purl.uniprot.org/citations/11133517 | http://purl.uniprot.org/core/title | "Impaired solute accumulation in inner medulla of Clcnk1-/- mice kidney."xsd:string |
| http://purl.uniprot.org/citations/11133517 | http://purl.uniprot.org/core/volume | "280"xsd:string |
| http://purl.uniprot.org/citations/11133517 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/11133517 |
| http://purl.uniprot.org/citations/11133517 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/11133517 |
| http://purl.uniprot.org/uniprot/Q9WUB7#attribution-D15267564CB3247B9C3D8CA7CEA4643B | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/11133517 |
| http://purl.uniprot.org/uniprot/#_A2ADB4-mappedCitation-11133517 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11133517 |
| http://purl.uniprot.org/uniprot/#_Q9WUB7-mappedCitation-11133517 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11133517 |
| http://purl.uniprot.org/uniprot/A2ADB4 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/11133517 |
| http://purl.uniprot.org/uniprot/Q9WUB7 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/11133517 |