Uptake of Pi in basolateral vesicles after release of unilateral ureteral obstruction

1984 ◽  
Vol 247 (4) ◽  
pp. F543-F547
Author(s):  
S. J. Schwab ◽  
S. Klahr ◽  
M. R. Hammerman
Keyword(s):  
Ureteral Obstruction ◽  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Unilateral Ureteral Obstruction ◽  
Proximal Tubular Cell ◽  
Tubular Cell ◽  
Luminal Membrane ◽  
Pi Transport ◽  
Proximal Tubular

We previously demonstrated Na+-dependent 32Pi uptake in basolateral membrane vesicles from kidneys of normal dogs. We postulated that this reflects Na+-dependent Pi transport across the basolateral membrane into the proximal tubular cell in vivo that subserves cellular needs for Pi. To ascertain whether Pi transport across the basolateral membrane was enhanced in a condition in which delivery of Pi across the luminal membrane would be markedly decreased, we measured Na+-dependent 32Pi uptake in basolateral vesicles isolated from postobstructed and control kidneys of dogs following release of unilateral ureteral obstruction. Clearance of creatinine and filtered load of Pi were significantly decreased in postobstructed compared with control kidneys. Na+-dependent 32Pi uptake was increased in basolateral vesicles from postobstructed compared with control kidneys, as reflected by increased initial rate of uptake and an increased overshoot of 32Pi transport. Our findings are consistent with an adaptation resulting in increased transport of Pi across the basolateral membrane of the proximal tubular cell in unilateral ureteral obstruction. This process may provide required Pi to the cell under conditions in which decreased Pi is available for transport across the brush border membrane.

Electrogenic Na+-independent Pi transport in canine renal basolateral membrane vesicles

1986 ◽  
Vol 250 (3) ◽  
pp. F419-F424 ◽  
Author(s):  
S. J. Schwab ◽  
M. R. Hammerman
Keyword(s):  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Proximal Tubular Cell ◽  
Tubular Cell ◽  
Basolateral Membrane Vesicles ◽  
Luminal Membrane ◽  
Pi Transport ◽  
Dog Kidney ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

To define the mechanism by which Pi exists from the renal proximal tubular cell across the basolateral membrane, we measured 32Pi uptake in basolateral membrane vesicles from dog kidney in the absence of Na+. Preloading of basolateral vesicles with 2 mM Pi transstimulated 32Pi uptake, which is consistent with counterflow. We used measurements of transstimulation to quantitate the transport component of 32Pi uptake. Transstimulation of 32Pi uptake was inhibited less than 30% by concentrations of probenecid as high as 50 mM. In contrast, transstimulation of 35SO4(2-) uptake by intravesicular SO4(2-) was inhibited 92% by 5 mM probenecid. Preloading basolateral vesicles with SO4(2-) did not result in transstimulation of 32Pi uptake. Accumulation of 32Pi in basolateral vesicles above steady state was driven by a membrane potential (intravesicular positive), consistent with Na+-independent Pi transport being accompanied by the net transfer of negative charge across the membrane. We conclude that carrier-mediated, electrogenic Na+-independent 32Pi transport can be demonstrated in basolateral vesicles from dog kidney. This process appears to be mediated, at least in part, via a mechanism different from that by which SO4(2-) is transported. Electrogenic Na+-independent Pi transport may reflect one means by which Pi reabsorbed across the luminal membrane exists from the proximal tubular cell down an electrochemical gradient.

Uptake of Pi in brush border vesicles after release of unilateral ureteral obstruction

1982 ◽  
Vol 243 (1) ◽  
pp. F29-F35
Author(s):  
S. Weinreb ◽  
K. A. Hruska ◽  
S. Klahr ◽  
M. R. Hammerman
Keyword(s):  
Brush Border ◽  
Ureteral Obstruction ◽  
Membrane Vesicles ◽  
Fractional Excretion ◽  
Unilateral Ureteral Obstruction ◽  
Renal Tubular Cells ◽  
Pi Transport ◽  
Renal Tubular ◽  
And Control

After release of complete unilateral ureteral obstruction, a decreased fractional excretion of phosphate (Pi) is observed in the postobstructed kidney compared with the nonobstructed (control) kidney. To determine whether this decrease in the urinary excretion of Pi is due to changes in Na+-dependent Pi transport across the renal brush border membranes of postobstructed and control kidneys, membrane vesicles were prepared from the brush borders of kidneys from dogs that had undergone complete unilateral ureteral obstruction. Alkaline phosphatase activity was decreased in membrane vesicles isolated from postobstructed kidneys. No differences were observed in Na+-dependent Pi transport or in Na+ uptake in membrane vesicles isolated from postobstructed as compared with control kidneys. The in vivo administration of parathyroid hormone decreased Na+-dependent Pi transport in membrane vesicles isolated from postobstructed and control kidneys despite the absence of a phosphaturic response. Our findings suggest that no intrinsic change in the transport characteristics of Pi across the luminal membrane of renal tubular cells occurs with unilateral ureteral obstruction. The findings are consistent with the suggestion that the low fractional excretion of Pi in the postobstructed kidney results from very low filtered loads of Pi on the postobstructed side.

Glutamine transport in basolateral vesicles from dogs with acute respiratory acidosis

1984 ◽  
Vol 247 (3) ◽  
pp. F403-F407 ◽  
Author(s):  
D. W. Windus ◽  
S. Klahr ◽  
M. R. Hammerman
Keyword(s):  
Basolateral Membrane ◽  
Respiratory Acidosis ◽  
Membrane Vesicles ◽  
Proximal Tubular Cell ◽  
Tubular Cell ◽  
Basolateral Membrane Vesicles ◽  
Renal Proximal Tubular Cell ◽  
Glutamine Transport ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

It has been shown that acute respiratory acidosis in dogs results in enhanced renal extraction of L-glutamine from plasma and increased ammonia excretion per nephron. To determine whether a component of the enhanced L-glutamine extraction results from increased transport of L-glutamine across the basolateral membrane into the renal proximal tubular cell, we measured Na+ gradient-dependent L-[3H]glutamine transport in proximal tubular basolateral membrane vesicles isolated from kidneys of normal dogs and from kidneys of dogs following 2 h of acute respiratory acidosis. The initial rate of Na+ gradient-dependent L-[3H] glutamine uptake (15 s) was increased significantly in basolateral membrane vesicles from the acidotic compared with normal dogs. Increased uptake could be measured under conditions in which changes in membrane potential resulting from fluxes of solute were minimized. We conclude that an adaptation occurs in the basolateral membrane of the renal proximal tubular cell during acute respiratory acidosis that allows increased transport of L-glutamine across the membrane into the proximal tubular cell. This adaptation may permit increased ammonia production per nephron.

Interaction of insulin with the renal proximal tubular cell

1985 ◽  
Vol 249 (1) ◽  
pp. F1-F11 ◽  
Author(s):  
M. R. Hammerman
Keyword(s):  
Basolateral Membrane ◽  
Tubular Epithelial Cell ◽  
Proximal Tubular Cell ◽  
Tubular Cell ◽  
Factor Ii ◽  
Renal Proximal Tubular Cell ◽  
Proximal Tubular ◽  
Hormonal Action ◽  
Specific Receptors ◽  
Renal Proximal Tubular

Insulin is known to regulate both metabolic and transport functions in the renal proximal tubule. Insulin present in plasma and in glomerular ultrafiltrate is known to be degraded at this nephron site. This paper summarizes what is known about these processes and about the mechanisms by which the actions of insulin and the degradation of insulin are effected in the proximal tubular epithelial cell. Recent studies have characterized the binding of insulin to specific receptors present in the proximal tubular basolateral membrane. Binding of insulin to its receptor in this membrane is thought to initiate events that lead to the phosphorylation of that receptor. Such insulin-stimulated phosphorylation may mediate hormonal action. A possible role for insulin-like growth factor II in the modulation of the actions of insulin has been suggested by observations in the kidney and in nonrenal cells. These findings are integrated into a model characterizing the nature of the interaction of insulin with the renal proximal tubular cell.

Calcium-activated phospholipase C associated with canine renal basolateral membranes

1987 ◽  
Vol 252 (1) ◽  
pp. F74-F82
Author(s):  
S. A. Rogers ◽  
M. R. Hammerman
Keyword(s):  
Phospholipase C ◽  
Basolateral Membrane ◽  
Proximal Tubular Cell ◽  
Tubular Cell ◽  
Free Calcium ◽  
Basolateral Membranes ◽  
Renal Proximal Tubular Cell ◽  
Dog Kidney ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

To determine whether calcium-activated phospholipase C effects breakdown of phospholipids present in the basolateral membrane of the renal proximal tubular cell we incubated proximal tubular basolateral membranes isolated from dog kidney in the absence and presence of deoxycholate, and varied free calcium from 0 to 300 microM. Following incubations, lipids were extracted from membranes and separated using thin-layer chromatography. In the absence of deoxycholate, neither phosphatidylinositol nor diglyceride extractable from basolateral membranes changed significantly as calcium was increased. In the presence of deoxycholate, extractable phosphatidylinositol and diglyceride did not change significantly as free calcium was elevated from 0 to 0.03 microM, but phosphatidylinositol decreased and diglyceride increased progressively as 0.03-300 microM free calcium was included in incubations. Most of the increased extractable diglyceride could be accounted for by hydrolysis of phosphatidylinositol as reflected by decreased extractable phosphatidylinositol. Our findings suggest that calcium-activated phospholipase C effects breakdown of phospholipids present in the basolateral portion of the plasma membrane of the renal proximal tubular cell. It is possible that this enzyme plays a role in stimulating protein kinase c at this site.

Binding of IGF I and IGF I-stimulated phosphorylation in canine renal basolateral membranes

1986 ◽  
Vol 251 (1) ◽  
pp. E32-E41 ◽  
Author(s):  
M. R. Hammerman ◽  
J. R. Gavin
Keyword(s):  
Insulin Receptor ◽  
Basolateral Membrane ◽  
Proximal Tubular Cell ◽  
Membrane Receptors ◽  
Tubular Cell ◽  
Basolateral Membranes ◽  
Renal Proximal Tubular Cell ◽  
Igf I ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

To characterize the interaction of the renal proximal tubular cell with insulin like growth factor I (IGF I), we measured binding of 125I-IGF I to proximal tubular basolateral membranes from dog kidney and induced IGF I-stimulated phosphorylation of basolateral membranes. Specific binding of 125I-IGF I to basolateral membranes was observed that was half-maximal at between 10(-9) and 10(-8) M IGF I. 125I-IGF I was affinity cross-linked to a 135,000 Mr protein in basolateral membranes that was distinct from the alpha-subunit of the insulin receptor and from the IGF II receptor. IGF I-stimulated phosphorylation of a 92,000 Mr protein was effected in detergent-solubilized membranes incubated with 100 microM [gamma-32P]ATP. The 32P-labeled protein was distinct from the beta-subunit of the insulin receptor, the 32P phosphorylation of which was stimulated by insulin. We conclude that specific receptors for IGF I are present in the basolateral membrane of the renal proximal tubular cell. Physiological actions of IGF I at this nephron site may occur through the binding of this peptide circulating in plasma, to specific basolateral membrane receptors, followed by IGF I stimulated phosphorylation.

scholarly journals Plasmatic Villin 1 Is a Novel In Vivo Marker of Proximal Tubular Cell Injury During Renal Ischemia-Reperfusion

2017 ◽  
Vol 101 (11) ◽  
pp. e330-e336 ◽  
Author(s):  
Jean-Paul Decuypere ◽  
Laurens J. Ceulemans ◽  
Tine Wylin ◽  
Wim Martinet ◽  
Diethard Monbaliu ◽  
...  
Keyword(s):  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Proximal Tubular Cell ◽  
Renal Ischemia ◽  
Tubular Cell ◽  
Proximal Tubular

Decreased luminal membrane transport of phosphate in chronic renal failure

1982 ◽  
Vol 242 (1) ◽  
pp. F17-F22 ◽  
Author(s):  
K. A. Hruska ◽  
S. Klahr ◽  
M. R. Hammerman
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Brush Border Membrane ◽  
Renal Tubule ◽  
Membrane Vesicles ◽  
Luminal Membrane ◽  
Pi Transport ◽  
Proximal Tubular ◽  
22Na Uptake ◽  
Renal Proximal Tubular

To examine the effects of the hyperparathyroidism that accompanies chronic renal failure (CRF) on Pi transport across the renal proximal tubular luminal membrane, brush border membrane vesicles (BBMV) were prepared from the viable portion of the kidney of dogs with CRF or normal renal function. Initial rates of Na+ gradient-dependent Pi transport were decreased in BBMV from dogs with CRF compared with normal dogs. Initial rates of 22Na+ uptake in BBMV from dogs with CRF, however, were increased, suggesting a more rapid dissipation of the Na+ gradient in these vesicles. Initial rates of Pi transport measured under Na+-equilibrated conditions were decreased in BBMV from dogs with CRF. Parathyroidectomy of dogs with CRF abolished this decrease in Pi uptake. We conclude that the adaptations in Pi excretion associated with CRF are accompanied by changes in Na+-dependent Pi transport in BBMV and, therefore, possibly across the luminal membrane of the renal tubule. Moreover, the activity of this transport system can be altered by parathyroidectomy of dogs prior to isolation of BBMV.

scholarly journals Overexpressed cyclophilin B suppresses aldosterone-induced proximal tubular cell injury both in vitro and in vivo

Oncotarget ◽  
2016 ◽  
Vol 7 (43) ◽  
pp. 69309-69320 ◽  
Author(s):  
Bin Wang ◽  
Lilu Lin ◽  
Haidong Wang ◽  
Honglei Guo ◽  
Yong Gu ◽  
...  
Keyword(s):  
Cell Injury ◽  
Proximal Tubular Cell ◽  
Tubular Cell ◽  
Cyclophilin B ◽  
Proximal Tubular
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