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Role of UTB Urea Transporters in the Urine Concentrating Mechanism of the Rat Kidney
Author(s) -
Layton Anita T
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.840.1
Subject(s) - urea , chemistry , urine osmolality , medullary cavity , kidney , endocrinology , renal medulla , medicine , urine , tubular fluid , biochemistry , biology , reabsorption
A new, region‐based mathematical model of the renal medulla of the rat kidney was used to investigate urine concentrating mechanism function in animals lacking the UTB urea transporter. The wild‐type model configuration generated an osmolality gradient along the cortico‐medullary axis that is consistent with measurements from rats in a moderately antidiuretic state. When expression of UTB was eliminated, model results indicated that the outer‐medullary (OM) cortico‐medullary osmolality gradient and the net urea flow through the OM were little affected. However, because urea transfer from ascending to descending vasa recta was much reduced, urea trapping by countercurrent exchange was significantly compromised. Consequently, urine urea concentration and osmolality were significantly decreased from model wild‐type, with most of the reduction attributable to the impaired inner‐medullary (IM) concentrating mechanism. These results indicate that the in vivo urine concentrating defect in knockout mouse is not attributable to an OM concentrating mechanism defect, but that reduced urea trapping by long vasa recta plays a significant role in compromising the concentrating mechanism of the IM. This research was supported in part by NIH grant DK‐89066 and by NSF grant DMS‐0715021.

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