Glutathione-dependent inactivation of sodium-dependent phosphate transport across rat renal brush-border membrane

1989 ◽  
Vol 413 (4) ◽  
pp. 329-335 ◽  
Author(s):  
Makoto Suzuki ◽  
Takeo Iwamoto ◽  
Yoshindo Kawaguchi ◽  
Keiji Iriyama ◽  
Aiichirou Ogawa ◽  
...  
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Phosphate Transport ◽  
Renal Brush Border Membrane ◽  
Dependent Inactivation ◽  
Sodium Dependent ◽  
Renal Brush Border

Effect of ischemia-reperfusion on the renal brush-border membrane sodium-dependent phosphate cotransporter NaPi-2

2001 ◽  
Vol 79 (3) ◽  
pp. 206-212 ◽  
Author(s):  
Yansen Xiao ◽  
Richard R Desrosiers ◽  
Richard Béliveau
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Ischemia Reperfusion ◽  
Phosphate Transport ◽  
Renal Ischemia ◽  
Ischemia And Reperfusion ◽  
Renal Brush Border Membrane ◽  
Sodium Dependent ◽  
And Function ◽  
Renal Brush Border

To understand the mechanisms underlying ischemia-reperfusion-induced renal proximal tubule damage, we analyzed the expression of the Na+-dependent phosphate (Na+/Pi) cotransporter NaPi-2 in brush border membranes (BBM) isolated from rats which had been subjected to 30 min renal ischemia and 60 min reperfusion. Na+/Pi cotransport activities of the BBM vesicles were also determined. Ischemia caused a significant decrease (about 40%, P < 0.05) in all forms of NaPi-2 in the BBM, despite a significant increase (31 ± 3%, P < 0.05) in the Na+/Pi cotransport activity. After reperfusion, both NaPi-2 expression and Na+/Pi cotransport activity returned to control levels. In contrast with Na+/Pi cotransport, ischemia significantly decreased Na+-dependent glucose cotransport but did not affect Na+-dependent proline cotransport. Reperfusion caused further decreases in both Na+/glucose (by 60%) and Na+/proline (by 33%) cotransport. Levels of NaPi-2 were more reduced in the BBM than in cortex homogenates, suggesting a relocalization of NaPi-2 as a result of ischemia. After reperfusion, NaPi-2 levels returned to control values in both BBM and homogenates. These data indicate that the NaPi-2 protein and BBM Na+/Pi cotransport activity respond uniquely to reversible renal ischemia and reperfusion, and thus may play an important role in maintaining and restoring the structure and function of the proximal tubule.Key words: kidney, ischemia, reperfusion, phosphate, transport.

Lactate-sodium cotransport in rat renal brush border membranes

1980 ◽  
Vol 239 (5) ◽  
pp. F496-F506 ◽  
Author(s):  
M. Barac-Nieto ◽  
H. Murer ◽  
R. Kinne
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Choline Chloride ◽  
Precipitation Method ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Renal Brush Border Membrane ◽  
Sodium Dependent ◽  
Lactate Uptake ◽  
Renal Brush Border

Brush border membrane vesicles were obtained from rat kidney cortex through a calcium precipitation method and their transport properties for lactate were studied by a rapid-filtration technique. Transient concentrative uptake of L-lactate was observed in the presence of inwardly directed NaCl gradient, but not in the presence of a KCl, LiCl, RbCl, CsCl, or choline chloride gradient. The sodium-dependent L-lactate uptake was saturable and was inhibited by D-lactate. The activation curve with sodium was hyperbolic. Maneuvers that render the inside of the vesicle more negative stimulated sodium-dependent L-lactate uptake, suggesting an electrogenic transfer of L-lactate and sodium. An L-lactate gradient also accelerates the sodium movement across the brush border membrane. Studies on the pH dependency of L-lactate transport and on the effect of L-lactate on proton movements across the brush border membrane indicate that there is little contribution of nonionic diffusion and/or of lactate-H+ cotransport to the transfer of L-lactate across the renal brush border membrane. In summary, sodium-lactate cotransport is the major mechanism for L-lactate transfer across the renal brush border membrane.

Chloride dependency of renal brush-border membrane phosphate transport

1999 ◽  
Vol 277 (4) ◽  
pp. F506-F512
Author(s):  
Norimoto Yanagawa ◽  
Chi Pham ◽  
Remi N. J. Shih ◽  
Stephen Miao ◽  
Oak Don Jo
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Electrical Potential ◽  
Phosphate Transport ◽  
P Uptake ◽  
Niflumic Acid ◽  
Renal Brush Border Membrane ◽  
Transport Inhibitors ◽  
Transmembrane Electrical Potential ◽  
Renal Brush Border

In our present study, we examined the effect of Cl− on rabbit renal brush-border membrane (BBM) phosphate (Pi) uptake. It was found that the Na+-dependent BBM32P uptake was significantly inhibited by Cl− replacement in the uptake solution with other anions, or by Cl− transport inhibitors, including DIDS, SITS, diphenylamine-2-carboxylate (DPC), niflumic acid (NF), and 5-nitro-2-(3-phenylpropylamino)benzoate (NPPB). Intravesicular formate or Cl− increased BBM36Cl−uptake but did not affect BBM 32P uptake. BBM22Na+uptake was lowered by Cl−replacement in the uptake solution but not by Cl− transport inhibitors. Changes in transmembrane electrical potential altered BBM36Cl−and 32P uptake in directions consistent with a net inward movement of negative and positive charges, respectively. However, the Cl−-dependent BBM Pi uptake was not affected by changes in transmembrane electrical potential. Finally, a similar Cl− dependency of Pi uptake was also found with BBM derived from rat and mouse kidneys. In summary, our study showed that a component of Na+-dependent Pi uptake was also Cl− dependent in rabbit, rat, and mouse renal BBM. The mechanism underlying this Cl− dependency remains to be identified.

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