Effect of Parathyroid-Hormone-Related Protein on Sodium-Dependent Phosphate Transport in Renal Brush Border Membrane Vesicles in Rats

Renal clearance studies showed that parathyroidectomy (PTX) stimulated renal PO4 reabsorption within 90 min in 3-wk-old chicks. Subsequent parathyroid hormone (PTH) infusion caused net PO4 secretion. Kidneys were taken for brush-border membrane (BBM) preparations 3 h after PTX or sham operations and 1 h after PTH or saline injections, thus yielding four categories of PTH status: PTX/saline, sham/saline, PTX/PTH, and sham/PTH. Efficacy of PTX and PTH was confirmed by examination of serum Ca concentrations. A 100 mM NaSCN gradient, out greater than in, caused concentrative PO4 uptake by BBM from sham/saline animals. Concentrative uptake was not produced by 100 mM KSCN, out greater than in; pH 7.4in vs. pH 5.4out; or 100 mM NaC1, out = in. Removal of endogenous PTH (PTX/saline) significantly stimulated Na-dependent PO4 uptake compared with sham/saline. PTH infusion significantly depressed Na-dependent PO4 uptake in PTX/PTH and sham/PTH groups compared with sham/saline and PTX/saline. Na-dependent, concentrative glucose uptake was present and unchanged by PTH. Kinetic analysis, based on 5-s uptakes, showed that both apparent affinity and maximal velocity (Vmax) for Na-dependent PO4 transport were decreased by PTH treatment. The data suggest that PTH influences avian renal PO4 excretion at least in part through a Na-dependent PO4 transport system in proximal tubule BBM.

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Stimulation of calcium uptake by parathyroid hormone in renal brush-border membrane vesicles. Relationship to membrane phosphorylation.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(17)43875-0 ◽

1983 ◽

Vol 258 (23) ◽

pp. 14400-14406

Author(s):

S Khalifa ◽

S Mills ◽

K A Hruska

Keyword(s):

Parathyroid Hormone ◽

Brush Border ◽

Calcium Uptake ◽

Brush Border Membrane ◽

Membrane Vesicles ◽

Brush Border Membrane Vesicles ◽

Renal Brush Border Membrane ◽

Membrane Phosphorylation ◽

Stimulation Of ◽

Renal Brush Border

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

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y00-122 ◽

2001 ◽

Vol 79 (3) ◽

pp. 206-212 ◽

Cited By ~ 4

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.

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