X-Linked Hypophosphatemia is a Disorder of Phosphate Transport in the Renal Brush Border Membrane in the Hypophosphatemic Mouse. Why is Serum 1,25-(OH)2D Low in the Human Homologue?

1979 ◽  
pp. 925-932
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Phosphate Transport ◽  
Human Homologue ◽  
Renal Brush Border Membrane ◽  
Renal Brush Border

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.

Parathyroid hormone effect on chicken renal brush-border membrane phosphate transport

1984 ◽  
Vol 247 (2) ◽  
pp. R302-R307 ◽  
Author(s):  
J. L. Renfro ◽  
N. B. Clark
Keyword(s):  
Parathyroid Hormone ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Phosphate Transport ◽  
Maximal Velocity ◽  
Apparent Affinity ◽  
Renal Brush Border Membrane ◽  
Hormone Effect ◽  
Clearance Studies ◽  
Renal Brush Border

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.

Renal brush-border membrane Na(+)-sulfate cotransport: stimulation by thyroid hormone

1991 ◽  
Vol 261 (3) ◽  
pp. F420-F426 ◽  
Author(s):  
H. S. Tenenhouse ◽  
J. Lee ◽  
N. Harvey
Keyword(s):  
Thyroid Hormone ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Phosphate Transport ◽  
Competitive Inhibitor ◽  
Maximal Velocity ◽  
Sulfate Transport ◽  
Renal Brush Border Membrane ◽  
Phosphate Cotransport ◽  
Renal Brush Border

The present study was undertaken to examine the interaction of phosphonoformic acid (PFA) with the Na(+)-sulfate cotransporter and the effect of thyroid hormone (triiodothyronine; T3) on Na(+)-dependent sulfate transport and Na(+)-dependent PFA binding in mouse renal brush-border membrane vesicles. PFA inhibits Na(+)-dependent sulfate transport in a competitive manner [apparent inhibitory constant (Ki) = 4.3 +/- 1.1 mM]. T3 administered in pharmacological doses significantly stimulates Na(+)-dependent sulfate transport in renal brush-border membranes compared with vehicle-treated controls. Although T3 has no effect on Na(+)-dependent glucose transport, T3 also stimulates Na(+)-dependent phosphate transport. Kinetic studies demonstrate that T3 increases the apparent maximal velocity (Vmax) for Na(+)-sulfate cotransport without changing the apparent Michaelis constant (Km). T3 does not significantly affect either Na(+)-dependent PFA binding or the phosphate- and sulfate-displaceable components of Na(+)-dependent PFA binding. Finally, Na(+)-dependent brush-border membrane sulfate transport is unchanged in phosphate-deprived mice that exhibit increased Na(+)-phosphate cotransport and in X-linked Hyp mice that exhibit impaired Na(+)-phosphate cotransport. The present results demonstrate that 1) PFA is a competitive inhibitor of Na(+)-sulfate cotransport, 2) T3 stimulates Na(+)-dependent sulfate, as well as Na(+)-dependent phosphate transport, but has no effect on PFA binding, and 3) phosphate deprivation and the X-linked Hyp mutation do not influence Na(+)-sulfate cotransport.(ABSTRACT TRUNCATED AT 250 WORDS)

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