Urine-concentrating mechanism in the inner medulla: function of the thin limbs of the loops of Henle.
Published
Journal Article
The ability of mammals to produce urine hyperosmotic to plasma requires the generation of a gradient of increasing osmolality along the medulla from the corticomedullary junction to the papilla tip. Countercurrent multiplication apparently establishes this gradient in the outer medulla, where there is substantial transepithelial reabsorption of NaCl from the water-impermeable thick ascending limbs of the loops of Henle. However, this process does not establish the much steeper osmotic gradient in the inner medulla, where there are no thick ascending limbs of the loops of Henle and the water-impermeable ascending thin limbs lack active transepithelial transport of NaCl or any other solute. The mechanism generating the osmotic gradient in the inner medulla remains an unsolved mystery, although it is generally considered to involve countercurrent flows in the tubules and vessels. A possible role for the three-dimensional interactions between these inner medullary tubules and vessels in the concentrating process is suggested by creation of physiologic models that depict the three-dimensional relationships of tubules and vessels and their solute and water permeabilities in rat kidneys and by creation of mathematical models based on biologic phenomena. The current mathematical model, which incorporates experimentally determined or estimated solute and water flows through clearly defined tubular and interstitial compartments, predicts a urine osmolality in good agreement with that observed in moderately antidiuretic rats. The current model provides substantially better predictions than previous models; however, the current model still fails to predict urine osmolalities of maximally concentrating rats.
Full Text
Duke Authors
Cited Authors
- Dantzler, WH; Layton, AT; Layton, HE; Pannabecker, TL
Published Date
- October 2014
Published In
Volume / Issue
- 9 / 10
Start / End Page
- 1781 - 1789
PubMed ID
- 23908457
Pubmed Central ID
- 23908457
Electronic International Standard Serial Number (EISSN)
- 1555-905X
International Standard Serial Number (ISSN)
- 1555-9041
Digital Object Identifier (DOI)
- 10.2215/CJN.08750812
Language
- eng