scholarly journals Corrigendum: Integrin Beta 1 Is Crucial for Urinary Concentrating Ability and Renal Medulla Architecture in Adult Mice

2018 ◽  
Vol 9 ◽  
Author(s):  
Anna Iervolino ◽  
Luigi R. De La Motte ◽  
Federica Petrillo ◽  
Federica Prosperi ◽  
Francesca Maria Alvino ◽  
...  
Keyword(s):  
Renal Medulla ◽  
Adult Mice ◽  
Urinary Concentrating Ability

scholarly journals Integrin Beta 1 Is Crucial for Urinary Concentrating Ability and Renal Medulla Architecture in Adult Mice

2018 ◽  
Vol 9 ◽  
Author(s):  
Anna Iervolino ◽  
Luigi R. De La Motte ◽  
Federica Petrillo ◽  
Federica Prosperi ◽  
Francesca Maria Alvino ◽  
...  
Keyword(s):  
Renal Medulla ◽  
Adult Mice ◽  
Urinary Concentrating Ability

Sequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney

2007 ◽  
Vol 292 (1) ◽  
pp. F269-F277 ◽  
Author(s):  
Hyun-Wook Lee ◽  
Wan-Young Kim ◽  
Hyun-Kuk Song ◽  
Chul-Woo Yang ◽  
Ki-Hwan Han ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Aldose Reductase ◽  
Vascular Endothelial Cells ◽  
Collecting Duct ◽  
Renal Medulla ◽  
Thick Ascending Limb ◽  
Urea Transporter ◽  
Adult Mice ◽  
Enhancer Binding Protein ◽  
Treatment Support

This study was conducted to test the hypothesis that, during renal development, the Na-K-2Cl cotransporter type 2 (NKCC2) activates the tonicity-responsive enhancer binding protein (TonEBP) transcription factor by creating medullary hypertonicity. TonEBP, in turn, drives the expression of aldose reductase (AR) and urea transporter-A (UT-A). Kidneys from 13- to19-day-old fetuses ( F13– F19), 1- to 21-day-old pups ( P1– P21), and adult mice were examined by immunohistochemistry. NKCC2 was first detected on F14 in differentiating macula densa and thick ascending limb (TAL). TonEBP was first detected on F15 in the medullary collecting duct (MCD) and surrounding endothelial cells. AR was detected in the MCD cells of the renal medulla from F15. UT-A first appeared in the descending thin limb (DTL) on F16 and in the MCD on F18. After birth, NKCC2-positive TALs disappeared gradually from the tip of the renal papilla, becoming completely undetectable in the inner medulla on P21. TonEBP shifted from the cytoplasm to the nucleus in both vascular endothelial cells and MCD cells on P1, and its abundance increased gradually afterward. Immunoreactivity for AR and UT-A in the renal medulla increased markedly after birth. Treatment of neonatal animals with furosemide dramatically reduced expression of TonEBP, AR, and UT-A1. Furosemide also prevented the disappearance of NKCC2-expressing TALs in the papilla. The sequential expression of NKCC2, TonEBP, and its targets AR and UT-A and the reduced expression TonEBP and its targets in response to furosemide treatment support the hypothesis that local hypertonicity produced by the activity of NKCC2 activates TonEBP during development.

Postnatal adrenalectomy impairs urinary concentrating ability by increased COX-2 and leads to renal medullary injury

2007 ◽  
Vol 293 (3) ◽  
pp. F780-F789 ◽  
Author(s):  
Jane Stubbe ◽  
Kirsten Madsen ◽  
Finn T. Nielsen ◽  
Rasmus K. Bonde ◽  
Ole Skøtt ◽  
...  
Keyword(s):  
Weight Gain ◽  
Extracellular Volume ◽  
Renal Medulla ◽  
Postnatal Period ◽  
Sham Operation ◽  
Volume Depletion ◽  
Rat Pups ◽  
Cox 2 ◽  
Urinary Concentrating Ability ◽  
Urine Concentrating Ability

We hypothesized that aldosterone promotes development of the renal medulla in the postnatal period and that cyclooxygenase-2 (COX-2) activity contributes to renal dysfunction after impaired aldosterone signaling. To test these hypotheses, rat pups underwent either sham operation or adrenalectomy at postnatal day 10. Adrenalectomized rats were divided into no steroid substitution (ADX), corticosterone replacement (ADX-C), and corticosterone and DOCA substitution (ADX-CD) groups that received subcutaneous pellets with steroids. Without replacement, pups failed to thrive and exhibited impaired urinary-concentrating ability. The renal medulla was significantly smaller, and the medullary interstitial osmolality was lower in the ADX group, whereas COX-2 and PGE2 tissue levels were significantly elevated compared with levels shown in sham animals. Substitution with DOCA and corticosterone corrected these changes, whereas corticosterone replacement alone improved survival but not weight gain and urinary-concentrating ability. Administration of a COX-2 inhibitor to ADX rats (parecoxib, 5 mg·kg−1·day−1, days 17–20) increased weight gain, urinary-concentrating ability, and papillary osmolality. After fluid deprivation, parecoxib attenuated weight loss and the increase in plasma Na+ concentration and osmolality. It is concluded that mineralocorticoid is required for normal postnatal development of the renal medulla. COX-2 contributes to impaired urine-concentrating ability, NaCl loss, and extracellular volume depletion in postnatal mineralocorticoid deficiency.

Renal medullary blood flow: its measurement and physiology

1986 ◽  
Vol 64 (7) ◽  
pp. 873-880 ◽  
Author(s):  
W. A. Cupples
Keyword(s):  
Blood Flow ◽  
Renal Medulla ◽  
Vascular Bundles ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Countercurrent Exchange ◽  
Renal Medullary Blood Flow ◽  
Urinary Concentrating Ability ◽  
Velocity Tracking ◽  
Uptake Method

The vasculature of the mammalian renal medulla is complex, having neither discrete input nor output. There is also efficient countercurrent exchange between ascending and descending vasa recta in the vascular bundles. These considerations have hampered measurement of medullary blood flow since they impose pronounced constraints on methods used to assess flow. Three main strategies have been used: (i) indicator extraction; (ii) erythrocyte velocity tracking; and (iii) indicator dilution. These are discussed with respect to their assumptions, requirements, and limitations. There is a consensus that medullary blood flow is autoregulated, albeit over a narrower pressure range than is total renal blood flow. When normalized to gram tissue weight, medullary blood flow in the dog is similar to that in the rat, on the order of 1 to 1.5 mL∙min−1∙g−1. This is considerably greater than estimated by the radioiodinated albumin uptake method which has severe conceptual and practical problems. From both theoretical and experimental evidence it ssems that urinary concentrating ability is considerably less sensitive to changes in medullary blood flow than is often assumed.

Urea and urine concentrating ability: new insights from studies in mice

2005 ◽  
Vol 288 (5) ◽  
pp. F881-F896 ◽  
Author(s):  
Baoxue Yang ◽  
Lise Bankir
Keyword(s):  
Renal Medulla ◽  
Wild Type ◽  
Urea Clearance ◽  
Renal Handling ◽  
Plasma Urea ◽  
Targeted Gene Deletion ◽  
Enhanced Expression ◽  
Urinary Concentrating Ability ◽  
Concentrate Urea ◽  
Urine Concentrating Ability

Urea is the most abundant solute in the urine in humans (on a Western-type diet) and laboratory rodents. It is far more concentrated in the urine than in plasma and extracellular fluids. This concentration depends on the accumulation of urea in the renal medulla, permitted by an intrarenal recycling of urea among collecting ducts, vasa recta and thin descending limbs, all equipped with specialized, facilitated urea transporters (UTs) (UT-A1 and 3, UT-B, and UT-A2, respectively). UT-B null mice have been recently generated by targeted gene deletion. This review describes 1) the renal handling of urea by the mammalian kidney; 2) the consequences of UT-B deletion on urinary concentrating ability; and 3) species differences among mice, rats, and humans related to their very different body size and metabolic rate, leading to considerably larger needs to excrete and to concentrate urea in smaller species (urea excretion per unit body weight in mice is 5 times that in rats and 23 times that in humans). UT-B null mice have a normal glomerular filtration rate but moderately reduced urea clearance. They exhibit a 30% reduction in urine concentrating ability with a more severe defect in the capacity to concentrate urea (50%) than other solutes, despite a twofold enhanced expression of UT-A2. The urea content of the medulla is reduced by half, whereas that of chloride is almost normal. When given an acute urea load, UT-B null mice are unable to raise their urinary osmolality, urine urea concentration (Uurea), and the concentration of non-urea solutes, as do wild-type mice. When fed diets with progressively increasing protein content (10, 20, and 40%), they cannot prevent a much larger increase in plasma urea than wild-type mice because they cannot raise Uurea. In both wild-type and UT-B null mice, urea clearance was higher than creatinine clearance, suggesting the possibility that urea could be secreted in the mouse kidney, thus allowing more efficient excretion of the disproportionately high urea load. On the whole, studies in UT-B null mice suggest that recycling of urea by countercurrent exchange in medullary vessels plays a more crucial role in the overall capacity to concentrate urine than its recycling in the loops of Henle.

scholarly journals Increased urinary concentrating ability of P2Y2 receptor null mice is associated with marked increase in protein abundances of AQP2 and UT‐A in renal medulla

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Bellamkonda K Kishore ◽  
Jeff M Sands ◽  
Donald E Kohan ◽  
Christopher F Martin ◽  
Yuqiang Ge ◽  
...  
Keyword(s):  
Renal Medulla ◽  
P2y2 Receptor ◽  
Urinary Concentrating Ability

Maturation of TonEBP expression in developing rat kidney

2004 ◽  
Vol 287 (5) ◽  
pp. F878-F885 ◽  
Author(s):  
Ki-Hwan Han ◽  
Seung Kyoon Woo ◽  
Wan-Young Kim ◽  
Soo-Hyun Park ◽  
Jung-Ho Cha ◽  
...  
Keyword(s):  
Target Genes ◽  
Kidney Development ◽  
Rat Kidney ◽  
Renal Medulla ◽  
Organic Osmolytes ◽  
Vasa Recta ◽  
Enhancer Binding Protein ◽  
Genes Encoding ◽  
Urinary Concentrating Ability

Tonicity-responsive enhancer binding protein (TonEBP) is a transcriptional activator of the Rel family. In the renal medulla, TonEBP stimulates genes encoding proteins involved in cellular accumulation of organic osmolytes, the vasopressin-regulated urea transporters (UT-A), and heat shock protein 70. To understand the role of TonEBP in the development of urinary concentrating ability, TonEBP expression during rat kidney development was investigated. In embryonic kidneys, TonEBP immunoreactivity was detected 16 days postcoitus in the cytoplasm of the endothelial cells surrounding the medullary collecting ducts (MCD). By 20 days, TonEBP was detected in most tubular profiles in the medulla, including the loop of Henle and MCD, and interstitial cells. The intensity of TonEBP immunoreactivity was much higher in the vasa recta than the tubules. In addition, immunoreactivity was localized predominantly to the cytoplasm. On postnatal day 1, two major changes were observed. TonEBP immunoreactivity shifted to the nucleus, and the intensity of TonEBP immunoreactivity of the tubules increased dramatically. These changes were associated with an increase in TonEBP and sodium- myo-inositol cotransporter mRNA abundance. Thereafter, TonEBP expression in tubular profiles increased moderately. The adult pattern of TonEBP expression was established at postnatal day 21 coincident with full maturation of the renal medulla. Thus expression of TonEBP in developing kidneys occurred predominantly in the medulla and preceded expression of its target genes, including UT-A. These data suggest that TonEBP contributes to the development of urine-concentrating ability.

Impaired urinary concentrating ability and cyclic AMP in K+-depleted rat kidney

1976 ◽  
Vol 231 (4) ◽  
pp. 1204-1208 ◽  
Author(s):  
N Beck ◽  
SK Webster
Keyword(s):  
Cyclic Amp ◽  
Rat Kidney ◽  
Renal Medulla ◽  
Pathogenic Role ◽  
Amp System ◽  
Urinary Cyclic Amp ◽  
Urinary Concentrating Ability ◽  
K Depletion ◽  
Concentrating Defect

The possibility that an alteration of the vasopressin-dependent cyclic AMP system plays a pathogenic role in the urinary concentrating defect in K+ depletion was investigated in the rat. The antidiuretic response to vasopressin was significantly less in K+-depleted rats. In these K+-depleted rats, the increase in urinary cyclic AMP excretion in response to vasopressin was also significantly less. However, repletion of K+ for 1 wk by feeding high-K+ diets restored the ability to increase urinary cyclic AMP excretion in response to vasopressin. In the in vitro incubation of renal medullary slices, the increase in cyclic AMP concentration in response to vasopressin was also significantly less in the slices obtained from K+-depleted rats than in those obtained from control rats. These findings suggest that, in K+ depletion, there is a reversible impairment of the vasopressin-dependent cyclic AMP system in the renal medulla; this impairment may play a pathogenic role in the urinary concentrating defect in K+ depletion.

Structure and concentrating ability in the avian kidney

1989 ◽  
Vol 256 (2) ◽  
pp. R501-R509 ◽  
Author(s):  
D. L. Goldstein ◽  
E. J. Braun
Keyword(s):  
Body Mass ◽  
Bird Species ◽  
Renal Medulla ◽  
Strongly Correlated ◽  
Interspecific Comparison ◽  
Significant Relation ◽  
Macaroni Penguin ◽  
Primary Determinant ◽  
Avian Kidney ◽  
Urinary Concentrating Ability

We quantified various aspects of the morphology of the kidney in seven bird species and related these measures to urinary concentrating ability (the concentration of ureteral urine in dehydrated animals) for six of the species. Kidney mass, number of glomeruli, and number of medullary cones all tended to increase with body mass. Smaller birds, with smaller kidneys, had smaller nephrons with smaller glomeruli. Lengths of medullary cones tended to increase with body mass and were exceptionally long in the macaroni penguin. The proportion of nephrons that were mammalian-type (MT, with loops of Henle) ranged from 7% (ring-necked pheasant) to 30% (zebra finch, glaucous-winged gull) and was unrelated to kidney mass. The percent of kidney mass comprised of medullary cones varied from 5 to 13%, unrelated to kidney mass. The number of reptilian-type (without loops of Henle) nephrons associated with each medullary cone tended to increase with kidney mass. Of the variables examined, length of the medullary cones, and hence of the longest loops of Henle, was most strongly correlated with urinary concentrating ability; however, this correlation was negative. Concentrating ability was also strongly negatively correlated with body mass (small birds concentrate better). No significant relation existed between concentrating ability and proportion of MT nephrons. Our data suggest that, in a broad interspecific comparison, the quantitative extent of the renal medulla is not the primary determinant of urinary concentrating ability in birds.

Urinary concentrating ability: insights from comparative anatomy

1985 ◽  
Vol 249 (6) ◽  
pp. R643-R666 ◽  
Author(s):  
L. Bankir ◽  
C. de Rouffignac
Keyword(s):  
Water Conservation ◽  
Comparative Anatomy ◽  
Renal Medulla ◽  
Urine Concentration ◽  
Vascular Bundles ◽  
High Concentration ◽  
Morphological Adaptations ◽  
Time Required ◽  
Urinary Concentrating Ability ◽  
Coherent Picture

It appears difficult to build a coherent picture of the concentrating system of the mammalian renal medulla. This may be due to the diversity of the factors involved and to considerable interspecies differences. Several morphological adaptations that may be critical in the improvement of water conservation are described. They include variations in the length of the papilla, number of nephrons, percentage of long-looped nephrons, nephron heterogeneity, development of pelvic fornices, confluence of collecting ducts, vascular bundles in the inner stripe of the outer medulla, thin descending limb epithelium, and relative development of the three medullary zones. The organization of the medullary circulation is described; the medulla includes several functionally different compartments favoring preferential exchanges by the juxtaposition of certain tubules and vessels. This may improve the efficiency of certain recycling routes and hence the insulation of the different compartments. As discussed in section III, a better inner medullary insulation may be key, not (or not only) in achieving a high urine concentration but mainly in reducing the time required to reach this high concentration. This overview of the multiple interspecies variations in medullary organization underlines the importance, among other factors, of the inner stripe architecture and of the internephron differences in the process of urine concentration.

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