Effect of acute ureteral obstruction on terminal collecting duct function in the weanling rat

1979 ◽  
Vol 236 (3) ◽  
pp. F260-F267 ◽  
Author(s):  
J. Buerkert ◽  
D. Martin ◽  
M. Head
Keyword(s):  
Ureteral Obstruction ◽  
Collecting Duct ◽  
Terminal Segment ◽  
Unilateral Ureteral Obstruction ◽  
Sodium Reabsorption ◽  
Loop Of Henle ◽  
Acute Obstruction ◽  
Reabsorptive Capacity ◽  
Weanling Rats

Micropuncture techniques were employed to evaluate the effects of unilateral ureteral obstruction (UUO) of 18 h duration on the function of the terminal collecting duct in weanling rats 90-120 min following release of obstruction. In control animals and after release of UUO, water and sodium reabsorption continued along the terminal segment of the collecting duct. Fractional delivery of water (FRH2O) and sodium (FRNa) to this segment was increased after release of UUO. A significantly greater amount of the FRH2O and FRNa was reabsorbed along the terminal collecting duct following release of obstruction than in controls. Potassium was not consistently reabsorbed or secreted in either group. Following release of UUO, the osmolality of collecting duct fluid was lower than in controls, but was not different from the osmolality of fluid obtained from the bend of the loop of Henle. The results suggest that the permeability to water and the reabsorptive capacity of the collecting duct are not altered by acute obstruction.

scholarly journals ASC in Renal Collecting Duct Epithelial Cells Contributes to Inflammation and Injury after Unilateral Ureteral Obstruction

2014 ◽  
Vol 184 (5) ◽  
pp. 1287-1298 ◽  
Author(s):  
Takanori Komada ◽  
Fumitake Usui ◽  
Koumei Shirasuna ◽  
Akira Kawashima ◽  
Hiroaki Kimura ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Ureteral Obstruction ◽  
Collecting Duct ◽  
Unilateral Ureteral Obstruction ◽  
Renal Collecting Duct

The control of sodium excretion

1978 ◽  
Vol 235 (3) ◽  
pp. F163-F173 ◽  
Author(s):  
H. E. de Wardener
Keyword(s):  
Proximal Tubule ◽  
Sodium Excretion ◽  
Collecting Duct ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Sodium Reabsorption ◽  
Loop Of Henle ◽  
Salt Loading ◽  
Large Fluctuations

The kidneys of a normal man filter approximately 24,000 meq sodium/day, reabsorb about 23,900, and yet can make a 1--2 meq change in 24-h urinary sodium excretion. The control of urinary sodium excretion, therefore, depends, first, on ensuring that the bulk of the sodium is reabsorbed, a function which is carried out in the proximal tubule and ascending loop of Henle. Second, it depends on adjusting the reabsorption of the small quantity of sodium which is delivered into the collecting duct so that the amount excreted in the urine is that required to maintain sodium balance. The bulk reabsorptive mechanisms can be considered as buffers to prevent large fluctuations in the amount of sodium delivered to the collecting duct, thus facilitating the fine adjustments of reabsorption which are made at this site. In conditions other than extreme salt loading or deprivation, changes in sodium reabsorption in the proximal tubule and loop of Henle probably have little, if any, effect on urinary sodium excretion. Sodium reabsorption in the proximal tubule and the collecting duct appears to be influenced by unidentified circulating substances.

scholarly journals INK4a knockout mice exhibit increased fibrosis under normal conditions and in response to unilateral ureteral obstruction

2010 ◽  
Vol 299 (6) ◽  
pp. F1486-F1495 ◽  
Author(s):  
Jesse M. Wolstein ◽  
David H. Lee ◽  
Jennine Michaud ◽  
Venessa Buot ◽  
Beth Stefanchik ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Knockout Mice ◽  
Ureteral Obstruction ◽  
Transforming Growth Factor ◽  
Mesangial Cells ◽  
Collecting Duct ◽  
Mesenchymal Cell ◽  
Transforming Growth Factor Β ◽  
Unilateral Ureteral Obstruction ◽  
Matrix Deposition

The INK4a proteins p16INK4a and p19ARF regulate cell cycle arrest and senescence. However, the role of these proteins in controlling these processes in the normal kidney and following injury is unknown. We performed unilateral ureteral obstruction (UUO) to induce fibrosis in 2- to 3-mo-old wild-type (WT) C57/B6 and INK4a knockout mice. By quantitative RT-PCR, p16INK4a levels were increased sixfold in WT mice 7 days after UUO and p19ARF remained undetectable. Kidney sections were examined to determine levels and localization of p16INK4a, apoptosis, fibrosis, and senescent cells. INK4a knockout mice displayed mesangial cell proliferation, increased matrix deposition, and myofibroblast differentiation under normal conditions. Following UUO, INK4a knockout mice displayed 10-fold increased tubular and interstitial cell proliferation, 75% decreased collecting duct apoptosis, 2-fold greater collagen and fibronectin deposition, and no cell senescence by senescence-associated β-galactosidase staining compared with WT mice. Both INK4a knockout mesangial cells and kidney lysates from knockout mice following injury showed elevated levels of IL-6 by ELISA compared with WT samples. INK4a knockout epithelial cell cultures displayed increased mesenchymal cell markers when exposed to transforming growth factor-β. These results confirm that p16INK4a controls cell proliferation and matrix production and mitigates fibrosis following injury and suggest that the mechanism involves a role in limiting inflammation and cell proliferation.

scholarly journals Deficiency of mPGES-1 exacerbates renal fibrosis and inflammation in mice with unilateral ureteral obstruction

2017 ◽  
Vol 312 (1) ◽  
pp. F121-F133 ◽  
Author(s):  
Renfei Luo ◽  
Yutaka Kakizoe ◽  
Feifei Wang ◽  
Xiang Fan ◽  
Shan Hu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Collecting Duct ◽  
Unilateral Ureteral Obstruction ◽  
Prostaglandin E ◽  
Expression Levels ◽  
Collagen Iii ◽  
Tgf Β1

Microsomal prostaglandin E2 synthase-1 (mPGES-1), an inducible enzyme that converts prostaglandin H2 to prostaglandin E2 (PGE2), plays an important role in a variety of inflammatory diseases. We investigated the contribution of mPGES-1 to renal fibrosis and inflammation in unilateral ureteral obstruction (UUO) for 7 days using wild-type (WT) and mPGES-1 knockout (KO) mice. UUO induced increased mRNA and protein expression of mPGES-1 and cyclooxygenase-2 in WT mice. UUO was associated with increased renal PGE2 content and upregulated PGE2 receptor (EP) 4 expression in obstructed kidneys of both WT and mPGES-1 KO mice; EP4 expression levels were higher in KO mice with UUO than those in WT mice. Protein expression of NLRP3 inflammasome components ASC and interleukin-1β was significantly increased in obstructed kidneys of KO mice compared with that in WT mice. mRNA expression levels of fibronectin, collagen III, and transforming growth factor-β1 (TGF-β1) were significantly higher in obstructed kidneys of KO mice than that in WT mice. In KO mice, protein expression of fibronectin and collagen III was markedly increased in obstructed kidneys compared with WT mice, which was associated with increased phosphorylation of protein kinase B (AKT). EP4 agonist CAY10598 attenuated increased expression of collagen I and fibronectin induced by TGF-β1 in inner medullary collecting duct 3 cells. Moreover, CAY10598 prevented the activation of NLRP3 inflammasomes induced by angiotensin II in human proximal tubule cells (HK2). In conclusion, these findings suggested that mPGES-1 exerts a potentially protective effect against renal fibrosis and inflammation induced by UUO in mice.

scholarly journals THE EFFECT OF UNILATERAL URETERAL OBSTRUCTION ON THE CONTRALATERAL RENAL GROWTH IN WEANLING RATS

1993 ◽  
Vol 84 (4) ◽  
pp. 747-756
Author(s):  
Shozo Ota ◽  
Ryuichiro Konda ◽  
Seiichi Orikasa ◽  
Satoru Kuji ◽  
Kiyohide Sakai ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Unilateral Ureteral Obstruction ◽  
Renal Growth ◽  
Weanling Rats

scholarly journals Aliskiren restores renal AQP2 expression during unilateral ureteral obstruction by inhibiting the inflammasome

2015 ◽  
Vol 308 (8) ◽  
pp. F910-F922 ◽  
Author(s):  
Weidong Wang ◽  
Renfei Luo ◽  
Yu Lin ◽  
Feifei Wang ◽  
Peili Zheng ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Protein Expression ◽  
Nlrp3 Inflammasome ◽  
Ureteral Obstruction ◽  
Collecting Duct ◽  
Unilateral Ureteral Obstruction ◽  
Renin Inhibitor ◽  
Inflammasome Activation ◽  
Mrna Levels ◽  
Direct Renin Inhibitor

Ureteral obstruction is associated with reduced expression of renal aquaporins (AQPs), urinary concentrating defects, and an enhanced inflammatory response, in which the renin-angiotensin system (RAS) may play an important role. We evaluated whether RAS blockade by a direct renin inhibitor, aliskiren, would prevent the decreased renal protein expression of AQPs in a unilateral ureteral obstruction (UUO) model and what potential mechanisms may be involved. UUO was performed for 3 days (3UUO) and 7 days (7UUO) in C57BL/6 mice with or without aliskiren injection. In 3UUO and 7UUO mice, aliskiren abolished the reduction of AQP2 protein expression but not AQP1, AQP3, and AQP4. mRNA levels of renal AQP2 and vasopressin type 2 receptor were decreased in obstructed kidneys of 7UUO mice, which were prevented by aliskiren treatment. Aliskiren treatment was also associated with a reduced inflammatory response in obstructed kidneys of UUO mice. Aliskiren significantly decreased mRNA levels of several proinflammatory factors, such as transforming growth factor-β and tumor necrosis factor-α, seen in obstructed kidneys of UUO mice. Interestingly, mRNA and protein levels of the NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome components apoptosis-associated speck-like protein containing a caspase recruitment domain, caspase-1, and IL-1β were dramatically increased in obstructed kidneys of 7UUO mice, which were significantly suppressed by aliskiren. In primary cultured inner medullary collecting duct cells, IL-1β significantly decreased AQP2 expression. In conclusions, RAS blockade with the direct renin inhibitor aliskiren increased water channel AQP2 expression in obstructed kidneys of UUO mice, at least partially by preventing NLRP3 inflammasome activation in association with ureteral obstruction.

Regulation of renal transport processes and hemodynamics by macrophages and lymphocytes

1990 ◽  
Vol 258 (4) ◽  
pp. F761-F767 ◽  
Author(s):  
G. F. Schreiner ◽  
D. E. Kohan
Keyword(s):  
Ureteral Obstruction ◽  
Immune Modulation ◽  
Immune Cell ◽  
Collecting Duct ◽  
Transport Processes ◽  
Renal Physiology ◽  
Sodium Reabsorption ◽  
Cell Physiology ◽  
Leukotriene D4 ◽  
Water Excretion

Inflammatory diseases of the renal glomerulus and interstitium are characterized by numerous alterations in renal glomerular hemodynamics and tubule transport processes. The cellular mechanisms underlying these changes have been theoretically attributed to nephron toxicity and destruction. However, recent studies suggest that many of the alterations in renal physiology may be mediated by specific immune cell-derived factors. Macrophages release a variety of cytokines on activation. One of these monokines, interleukin 1, induces a natriuresis by direct inhibition of collecting duct sodium reabsorption. Glomerular macrophages release highly vasoconstrictive compounds, including leukotriene D4 and thromboxane A2. Macrophages have now been demonstrated to migrate into the renal interstitium in diseases not previously considered to have an immunological component. Acute ureteral obstruction is characterized by a rapid infiltration of macrophages and lymphocytes into the kidney. Removal of the immune cell infiltrate in ureteral obstruction by irradiation markedly improves glomerular filtration rate and renal blood flow and partially corrects sodium and water excretion. Such immune modulation of renal function is likely to occur in a wide variety of diseases of the kidney, many of which do not involve a primary immunological insult. We propose that the abnormalities in renal hemodynamics and in the transport of fluid and electrolytes observed in states characterized by coexistence of immune cells among renal parenchymal cells may reflect a complex immune modulation of renal cell physiology.

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