How Renal Cells Handle Urea

Bagnasco, Serena M.

doi:10.1159/000016377

Cited by 17 publications

(8 citation statements)

References 38 publications

(40 reference statements)

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“…In mammals and fish, changes in UT mRNA expression under a variety of osmotic environments have been reported. Smith et al (Smith et al, 1995) and Bagnasco (Bagnasco, 2000) demonstrated that dehydration increases the expression of UT-A2 mRNA in rat kidney. Morgan et al (Morgan et al, 2003) found that renal osmolytes and urea concentration were decreased and that renal UT transcripts (SkUT) were significantly diminished in response to environmental dilution in a marine elasmobranch.…”

Section: Discussionmentioning

confidence: 99%

Effect of osmotic stress on expression of a putative facilitative urea transporter in the kidney and urinary bladder of the marine toad,Bufo marinus

Konno

Hyodo

Matsuda

et al. 2006

Journal of Experimental Biology

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SUMMARY Anuran amphibians accumulate a large amount of urea in their extracellular fluids to avoid a severe dehydration under dry and hyper-saline environments. To clarify the mechanisms of urea retention, we examined structure and distribution of the urea transporter (UT) in the kidney of the marine toad(Bufo marinus), and its expression in the kidney and urinary bladder following exposure to dry and hyper-saline conditions by means of cDNA cloning, semi-quantitative RT-PCR, immunoblot analysis and immunohistochemistry. The Bufo UT cDNA cloned from the kidney encodes a 390-amino-acid residue protein, which is 80% identical to Rana esculenta UT with the functional characteristics of a urea transporter. The Bufo UT mRNA was abundantly expressed in the kidney and urinary bladder, but not in the skin. In immunoblot analysis using a specific antibody raised against the Bufo UT, a 52 kDa protein similar to the glycosylated forms of mammalian UT-A2 (∼55 kDa) was detected in extracts from plasma membrane fractions of the kidney and urinary bladder. When toads were acclimated to dry and hyper-saline environments for 7 days, UT mRNA expression was upregulated in the kidney and urinary bladder and there was an elevated plasma urea concentration and osmolality. Immunohistochemistry showed that the UT was specifically localized on the apical membrane of the early distal tubule, known to be the diluting segment, in the kidney and the epithelial cells of urinary bladder. Immunoreactive cells were not detected along the late distal tubule, the connecting tubule or the collecting duct in the kidney. The present findings suggest that the Bufo UT probably contributes to urea transport in the kidney and urinary bladder in response to hyperosmotic stresses such as body fluid hypertonicity and dehydration.

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Section: Discussionmentioning

confidence: 99%

Effect of osmotic stress on expression of a putative facilitative urea transporter in the kidney and urinary bladder of the marine toad,Bufo marinus

Konno

Hyodo

Matsuda

et al. 2006

Journal of Experimental Biology

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“…Collecting system reabsorption of urea into the medullary interstitium is heavily involved in maintaining the interstitial osmotic gradient that underpins correct functioning of the countercurrent multiplier and urinary concentration [22]. Therefore, increased luminal and decreased interstitial concentrations of urea will contribute to increased urinary dilution independent of the loss of urea transporter expression.…”

Section: Discussionmentioning

confidence: 99%

Analysis of Urinary and Plasma Electrolytes in a Rat Model of Unilateral Ureteric Obstruction (UUO)

Quinlan¹,

Pérez‐Barriocanal²,

Wright³

et al. 2008

TOUNJ

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Abstract:Following unilateral ureteric obstruction (UUO), hydronephrosis is associated with long term reductions in renal blood flow (RBF) and glomerular filtration rate (GFR), tubular resistance to arginine-vasopressin (AVP), and reduced expression of aquaporin water channels and sodium (Na + ) and urea transporters. During UUO, renal function is contingent upon adaptive changes in the contralateral kidney. In the short term this response is associated with an increased GFR and a reduced expression of Na + transporters. We aimed to assess global renal function in UUO, including a comparison between the obstructed and non-obstructed kidneys.Adult male rats were subjected to UUO of either 3 or 10 days duration. Control rats underwent sham surgery. Before release of the ureteric ligature, blood and both bladder and obstructed renal pelvis urine was sampled, then both kidneys harvested. Urinary and plasma electrolytes and osmolality, and kidney weights, were measured.We observed i) mild uraemia in the obstructed animals, ii) extreme dilution of urine from the pelvis of the obstructed kidney in the absence of noteworthy alterations in plasma ions, and iii) evidence indicative of a contralateral diuresis/natriuresis.To the best of our knowledge, this is the first study simultaneously examining such an extensive range of urinary (bladder and obstructed renal pelvis) and plasma markers of renal function in UUO. The results demonstrate that UUO is associated with a small deterioration in overall renal function and marked changes in renal electrolyte handling, leading to changes in the composition of urinary output from both the non-obstructed and obstructed kidneys.

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“…13 Activation of KCC and stimulation of RVD occurs at concentrations of urea present in the renal medulla (100-600 mM). 45 Activation of KCC by urea is reversible, although volume reduction is not, so that progressive volume loss and CHC increase could occur during repetitive circulation through the kidney. The increase in sensitivity of SS RBCs to urea activation and the exaggerated volume reduction of SS reticulocytes in response to urea may contribute to the elevated CHCs observed in both SS reticulocytes and RBCs compared with AA cells.…”

Section: Discussionmentioning

confidence: 99%

Urea stimulation of KCl cotransport induces abnormal volume reduction in sickle reticulocytes

Joiner

Rettig

Jiang

et al. 2006

Blood

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KCl cotransport (KCC) activity contributes to pathologic dehydration in sickle (SS) red blood cells (RBCs). KCC activation by urea was measured in SS and IntroductionThe KCl cotransporter (KCC) mediates electroneutral coupled transport of K ϩ and Cl Ϫ in a variety of cell types. 1,2 KCC activation results in net efflux of KCl from cells with high potassium content, with accompanying water loss and volume reduction. KCC is active in reticulocytes and diminishes with red cell maturation. 3,4 It is thought to function physiologically to reduce red blood cell (RBC) volume and establish the high cellular hemoglobin concentration (CHC) characteristic of mature cells. KCC is activated in vitro by cell swelling, acid pH, sulfhydryl oxidation/alkylation, and exposure to urea, but the relative importance of these stimuli in vivo is unknown.In RBCs containing sickle hemoglobin (Hb S), KCC activity is high, in part because of the high percentage of reticulocytes. 4 However, Hb S or Hb C in trait RBCs (AS or AC) with normal mean cell age, or after incorporation into normal RBC ghosts, appears to increase KCC activity. 5,6 Expression of Hb S or C in transgenic mice also increases red cell KCC activity. 7 Recently, we demonstrated an abnormal response to acid pH in SS RBCs that was partially corrected by incubation with the sulfhydryl reducing agent, dithiothreitol. 8 These findings suggested that regulation of KCC is abnormal in SS RBCs.As a volume regulator, KCC activity is responsive to CHC. 9,10 KCC is activated on cell swelling, and, as KCl is lost, cell volume falls, cellular hemoglobin concentration increases, and transport activity diminishes. The resultant CHC thus reflects the physiologic "volume set point" of the system. The inactivation of KCC as the cell shrinks toward its new steady state is most likely a key factor in defining the volume regulatory function of the transporter, which in turn is crucial for establishing the steady state CHC for RBCs in vivo.Volume reduction mediated by KCC has been demonstrated with RBC density measurements. 7,11,12 However, these studies, like flux studies, are complicated by varying numbers of reticulocytes (or young cells) in unfractionated SS blood, which preclude comparisons of KCC-mediated volume reduction in SS and AA cells. We recently compared the RVD mediated by KCC and stimulated by cell swelling and acid pH in SS and AA reticulocytes by tracking the changes in reticulocyte CHC by means of density gradient analysis. 8 Acid-stimulated volume reduction was exaggerated in SS reticulocytes and was diminished by sulfhydryl reduction, parallel to the behavior of KCC flux activity. However, despite the normal response of KCC flux activation to cell swelling in SS RBCs, swelling-stimulated volume reduction was markedly abnormal in SS reticulocytes and resulted in higher final CHC than in AA reticulocytes. Thus, volume reduction and KCC fluxes appear to reflect different functional aspects of the KCC system in RBCs and may be subject to different pathologic influences in SS RBCs...

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How Renal Cells Handle Urea

Cited by 17 publications

References 38 publications

Effect of osmotic stress on expression of a putative facilitative urea transporter in the kidney and urinary bladder of the marine toad,Bufo marinus

Effect of osmotic stress on expression of a putative facilitative urea transporter in the kidney and urinary bladder of the marine toad,Bufo marinus

Analysis of Urinary and Plasma Electrolytes in a Rat Model of Unilateral Ureteric Obstruction (UUO)

Urea stimulation of KCl cotransport induces abnormal volume reduction in sickle reticulocytes

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