Sodium chloride, urea, and water transport in the thin ascending limb of Henle. Generation of osmotic gradients by passive diffusion of solutes.

Imai, Masashi; Kokko, Juha P.

doi:10.1172/jci107572

Cited by 188 publications

(75 citation statements)

References 19 publications

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“…The expression of ClC-K1 throughout each ATL apparently reflects the extremely high chloride permeability found in this segment (16). We assume that the prebend segment has a similar high chloride permeability.…”

Section: Three-dimensional Reconstructions Of Thin Limbs Of the Loopsmentioning

confidence: 73%

“…We assume that the prebend segment has a similar high chloride permeability. AQP1 is not expressed in the prebend segments or ATLs, reflecting the complete lack of osmotic water permeability in the ATLs (15,16,42) and, we assume, in the prebend segments as well. Both the DTLs and the ATLs have now been shown to have very high permeabilities to urea, but there is no evidence of known urea transporters to account for these (43,49).…”

Section: Three-dimensional Reconstructions Of Thin Limbs Of the Loopsmentioning

confidence: 99%

“…Although the ascending thin limbs (ATLs) in the IM, like the TALs in the outer medulla, have essentially no transepithelial osmotic water permeability (14-17), they also have no known active transepithelial transport of NaCl or any other solute (16,(18)(19)(20)(21). If this steep osmotic gradient in the IM is not generated by the same mechanism as the gradient in the outer medulla, how, then, is it generated?…”

Section: Introductionmentioning

confidence: 99%

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Urine-Concentrating Mechanism in the Inner Medulla

Dantzler

Layton

et al. 2014

Clinical Journal of the American Society of Nephrology

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SummaryThe 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 threedimensional 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.

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Section: Three-dimensional Reconstructions Of Thin Limbs Of the Loopsmentioning

confidence: 73%

Section: Three-dimensional Reconstructions Of Thin Limbs Of the Loopsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Urine-Concentrating Mechanism in the Inner Medulla

Dantzler

Layton

et al. 2014

Clinical Journal of the American Society of Nephrology

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“…In the outer medulla, the interstitial space is concentrated through the classic countercurrent multiplication mechanism (2) in which water and solute are separated by active NaCl transport from the water-impermeable thick ascending limb of Henle (3,4). However, in the IM the ascending portion of Henle's loop is incapable of high rates of active transport (5,6), implying that solute concentration in the IM occurs by a different, yet unknown mechanism.…”

mentioning

confidence: 99%

Urinary concentrating defect in mice with selective deletion of phloretin-sensitive urea transporters in the renal collecting duct

Fenton

Chou

Stewart

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

227

230

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To investigate the role of inner medullary collecting duct (IMCD) urea transporters in the renal concentrating mechanism, we deleted 3 kb of the UT-A urea transporter gene containing a single 140-bp exon (exon 10). Deletion of this segment selectively disrupted expression of the two known IMCD isoforms of UT-A, namely UT-A1 and UT-A3, producing UT-A1͞3 ؊/؊ mice. In isolated perfused IMCDs from UT-A1͞3 ؊/؊ mice, there was a complete absence of phloretin-sensitive or vasopressin-stimulated urea transport. On a normal protein intake (20% protein diet), UT-A1͞ 3 ؊/؊ mice had significantly greater fluid consumption and urine flow and a reduced maximal urinary osmolality relative to wildtype controls. These differences in urinary concentrating capacity were nearly eliminated when urea excretion was decreased by dietary protein restriction (4% by weight), consistent with the 1958 Berliner hypothesis stating that the chief role of IMCD urea transport in the concentrating mechanism is the prevention of ureainduced osmotic diuresis. Analysis of inner medullary tissue after water restriction revealed marked depletion of urea in UT-A1͞3 ؊/؊ mice, confirming the concept that phloretin-sensitive IMCD urea transporters play a central role in medullary urea accumulation. However, there were no significant differences in mean inner medullary Na ؉ or Cl ؊ concentrations between UT-A1͞3 ؊/؊ mice and wild-type controls, indicating that the processes that concentrate NaCl were intact. Thus, these results do not corroborate the predictions of passive medullary concentrating models stating that NaCl accumulation in the inner medulla depends on rapid vasopressin-regulated urea transport across the IMCD epithelium.UT-A ͉ isolated perfused tubule ͉ vasopressin ͉ concentrating mechanism F or survival remote from water sources, terrestrial animals require effective water-conservation mechanisms. In birds and mammals, water conservation depends on specialized urinary concentrating mechanisms that reduce water excretion while maintaining solute excretion. This concentrating function is carried out in the renal medulla. In mammals, the medulla is divided into two regions, the outer medulla and the inner medulla (IM), both of which manifest increased tissue osmolality relative to the blood plasma (1). In these regions, high interstitial osmolality draws water from the renal collecting duct via aquaporin water channels, resulting in a concentrated final urine. In the outer medulla, the interstitial space is concentrated through the classic countercurrent multiplication mechanism (2) in which water and solute are separated by active NaCl transport from the water-impermeable thick ascending limb of Henle (3, 4). However, in the IM the ascending portion of Henle's loop is incapable of high rates of active transport (5, 6), implying that solute concentration in the IM occurs by a different, yet unknown mechanism.One important feature of the IM that distinguishes it from the outer medulla is its ability to accumulate large amounts of urea. Berliner ...

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“…The ascending limbs of Henle's loop are impermeable to water [9,10], and the ALH System is modeled by …”

Section: The Boundary-value Problem Modeling the Renal Concentrating mentioning

confidence: 99%

The kidney model as an inverse problem

Breinbauer¹,

Lory

1991

Applied Mathematics and Computation

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The mammalian kidney is modeled by a multipoint boundary-value problem for a System of nonlinear ordinary differential equations. A corresponding inverse problem is presented, which allows the rigorous judgement of the potential of the given modeling technique. For its numerical Solution a discretization is proposed, which is tailor-made for kidney models. It leads to a nonlinear-programming problem with nonlinear equality and inequality constraints. The suggested methods are applied to current research problems in renal physiology.

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Sodium chloride, urea, and water transport in the thin ascending limb of Henle. Generation of osmotic gradients by passive diffusion of solutes.

Cited by 188 publications

References 19 publications

Urine-Concentrating Mechanism in the Inner Medulla

Urine-Concentrating Mechanism in the Inner Medulla

Urinary concentrating defect in mice with selective deletion of phloretin-sensitive urea transporters in the renal collecting duct

The kidney model as an inverse problem

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