Mechanisms of p-Aminohippurate transport by brush-border and basolateral membrane vesicles isolated from rat kidney cortex

1982 ◽  
Vol 692 (1) ◽  
pp. 97-100 ◽  
Author(s):  
Ryohei Hori ◽  
Mikihisa Takano ◽  
Tomonobu Okano ◽  
Shikifumi Kitazawa ◽  
Ken-Ichi Inui
Keyword(s):  
Brush Border ◽  
Rat Kidney ◽  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Kidney Cortex ◽  
Basolateral Membrane Vesicles ◽  
Rat Kidney Cortex

Indirect coupling to Na+ of p-aminohippuric acid uptake into rat renal basolateral membrane vesicles

1987 ◽  
Vol 253 (5) ◽  
pp. F795-F801 ◽  
Author(s):  
H. Shimada ◽  
B. Moewes ◽  
G. Burckhardt
Keyword(s):  
Transport System ◽  
Equilibrium Distribution ◽  
Rat Kidney ◽  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Kidney Cortex ◽  
Acid Uptake ◽  
Basolateral Membrane Vesicles ◽  
Rat Kidney Cortex ◽  
Indirect Coupling

Experiments with basolateral membrane vesicles prepared from rat kidney cortex were performed to study the mechanism by which p-aminohippuric acid (PAH) is taken up across the contraluminal membrane and is concentrated in proximal tubule cells. An inward Na+ gradient failed to stimulate [3H]PAH uptake compared with K+ or Li+ and did not cause intravesicular PAH accumulation above equilibrium distribution. In the absence of Na+, the dicarboxylates glutarate and suberate cis-inhibited and trans-stimulated [3H]PAH uptake, indicating a common transport system. In the presence of Na+, 10 microM glutarate in the incubation medium did not cis-inhibit, but rather stimulated [3H]PAH uptake and caused PAH accumulation above equilibrium distribution ("overshoot"). Li+ diminished this stimulation, but was without effect on [3H]PAH/PAH- and [3H]PAH/glutarate exchange. The data indicate the coexistence of a Na+ -coupled, Li+-sensitive transport system for dicarboxylates and a Li+ -insensitive PAH/dicarboxylate exchanger in the basolateral membrane. We propose that dicarboxylates are cotransported with Na+ into the cell and subsequently exchange for extracellular PAH at the basolateral membrane. PAH uptake is thereby indirectly coupled to Na+ via the Na+/dicarboxylate cotransporter.

scholarly journals Studies on the orientation of brush-border membrane vesicles

1978 ◽  
Vol 172 (1) ◽  
pp. 57-62 ◽  
Author(s):  
W Haase ◽  
A Schäfer ◽  
H Murer ◽  
R Kinne
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Rat Kidney ◽  
Freeze Fracture ◽  
Membrane Vesicles ◽  
Brush Border Membrane Vesicles ◽  
Immunological Methods ◽  
Kidney Cortex ◽  
Asymmetric Distribution ◽  
Rat Kidney Cortex

Orientation of rat renal and intestinal brush-border membrane vesicles was studied with two independent methods: electron-microscopic freeze-fracture technique and immunological methods. With the freeze-fracture technique a distinct asymmetric distribution of particles on the two membrane fracture faces was demonstrated; this was used as a criterion for orientation of the isolated membrane vesicles. For the immunological approach the accessibility or inaccessibility of aminopeptidase M localized on the outer surface of the cell membrane to antibodies was used. With both methods we showed that the brush-border membrane vesicles isolated from rat kidney cortex and from rat small intestine for transport studies are predominantly orientated right-side out.

Inhibition by phenylglyoxal of the sodium-coupled fluxes of glucose and phosphate in renal brush-border membranes

1988 ◽  
Vol 66 (9) ◽  
pp. 1005-1012 ◽  
Author(s):  
R. Béliveau ◽  
M. Bernier ◽  
S. Giroux ◽  
D. Bates
Keyword(s):  
Brush Border ◽  
Direct Method ◽  
Rat Kidney ◽  
Membrane Vesicles ◽  
Kidney Cortex ◽  
Sodium Influx ◽  
Rat Kidney Cortex ◽  
Process Modification ◽  
Arginine Residues ◽  
Phosphate Influx

The coupling of phosphate and glucose transport to sodium in brush-border membrane vesicles from rat kidney cortex was studied after chemical modification of arginine residues by phenylglyoxal. Phosphate (10 mM) and sodium (20 mM) uptakes were linear for 6 s and stimulated in the presence of their cosubstrate. The sodium: phosphate stoichiometry measured by a direct method was 1.74. Sodium-independent phosphate and glucose influx were found to be unaffected by phenylglyoxylation. Phosphate- or glucose-independent sodium influx also remained unaltered by the treatment. However, phosphate influx measured with sodium was inhibited by 69% and sodium influx measured with phosphate was inhibited by 40%. When these values were corrected for uncoupled fluxes, the sodium influx coupled to phosphate and the phosphate influx coupled to sodium were inhibited by 93 and 95%, respectively. Glucose influx measured in the presence of sodium was inhibited by 36% and sodium influx in the presence of glucose was reduced by 39%. When the values were corrected for diffusion, these inhibitions were 95 and 100%, respectively. We conclude that the coupling of phosphate and glucose to sodium fluxes by the renal carriers requires the participation of arginine residue(s) in the translocation process. Modification of this arginine by phenylglyoxal leads to a marked inhibition of coupling. These results suggest the implication of arginine residues in the molecular coupling for both glucose and phosphate sodium symporters.

Kinetic model for phosphate transport in renal brush-border membranes

1988 ◽  
Vol 254 (3) ◽  
pp. F329-F336 ◽  
Author(s):  
R. Beliveau ◽  
J. Strevey
Keyword(s):  
Brush Border ◽  
Rat Kidney ◽  
Membrane Vesicles ◽  
Phosphate Transport ◽  
Kidney Cortex ◽  
Binary Complex ◽  
Rat Kidney Cortex ◽  
First Time ◽  
Phosphate Influx ◽  
Phosphate Carrier

Phosphate transport was studied in brush-border membrane vesicles purified from rat kidney cortex. Influx and efflux were strongly dependent on the presence of cis sodium; the rate of efflux, calculated by linear regression performed on the first time points, was much lower than the rate of influx (0.044 vs. 0.198 pmol.microgram protein-1.s-1). Trans phosphate had a stimulatory effect on phosphate influx (145% stimulation at 10 mM phosphate trans, with 0.2 mM phosphate cis). Trans phosphate was, however, inhibitory for phosphate efflux (89% inhibition at 10 mM phosphate trans). Trans effects of sodium were also studied. With 200 mM trans sodium, we observed 73% inhibition of phosphate influx and 60% inhibition of phosphate efflux. Studies involving sodium and phosphate present at the same time as trans substrates showed that the trans inhibition of phosphate influx by sodium could be completely reversed by trans phosphate. Trans inhibition of phosphate efflux by phosphate was not additive to the inhibition caused by sodium. Addition of trans phosphate had a stimulatory effect on sodium-independent influx, indicating that the binary complex (C-P) could translocate in efflux. These results indicate that the renal phosphate carrier presents a random binding scheme for the intra- and extravesicular sides of the membrane.

scholarly journals Sulphate-ion/sodium-ion co-transport by brush-border membrane vesicles isolated from rat kidney cortex

1979 ◽  
Vol 182 (1) ◽  
pp. 223-229 ◽  
Author(s):  
Heinrich Lücke ◽  
Gertraud Stange ◽  
Heini Murer
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Rat Kidney ◽  
Electrical Potential ◽  
Membrane Vesicles ◽  
Brush Border Membrane Vesicles ◽  
Kidney Cortex ◽  
Electrical Potential Difference ◽  
Univalent Cations ◽  
Rat Kidney Cortex

Uptake of SO42− into brush-border membrane vesicles isolated from rat kindey cortex by a Ca2+-precipitation method was investigated by using a rapid-filtration technique. Uptake of SO42− by the vesicles was osmotically sensitive and represented transport into an intra-vesicular space. Transport of SO42− by brush-border membranes was stimulated in the presence of Na+, compared with the presence of K+ or other univalent cations. A typical ‘overshoot’ phenomenon was observed in the presence of an NaCl gradient (100mm-Na+ outside/zero mm-Na+ inside). Radioactive-SO42− exchange was faster in the presence of Na+ than in the presence of K+. Addition of gramicidin-D, an ionophore for univalent cations, decreased the Na+-gradient-driven SO42− uptake. SO42− uptake was only saturable in the presence of Na+. Counter-transport of Na+-dependent SO42− transport was shown with MoO42− and S2O32−, but not with PO42−. Changing the electrical potential difference across the vesicle membrane by establishing different diffusion potentials (anion replacement; K+ gradient±valinomycin) was not able to alter Na+-dependent SO42− uptake. The experiments indicate the presence of an electroneutral Na+/SO42−-co-transport system in brush-border membrane vesicles isolated from rat kidney cortex.

Inorganic anion transport in kidney and intestinal brush border and basolateral membranes

1980 ◽  
Vol 238 (6) ◽  
pp. F452-F460 ◽  
Author(s):  
S. Grinstein ◽  
R. J. Turner ◽  
M. Silverman ◽  
A. Rothstein
Keyword(s):  
Brush Border ◽  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Anion Transport ◽  
Significant Inhibition ◽  
Kidney Cortex ◽  
Basolateral Membrane Vesicles ◽  
Inorganic Anion ◽  
Transport Pathways ◽  
Basolateral Membranes

The efflux of inorganic anions from purified brush border and basolateral membrane vesicles from dog kidney cortex was measured under equilibrium exchange conditions. Marked differences in temperature sensitivity and effects of inhibitors were found between the Cl and SO4 transport pathways and between the two types of membranes. SO4 transport in both brush border and basolateral membranes was markedly reduced by cooling, but significant inhibition by 4,4'–diisothiocyano-2,2'–disulfonic stilbene (DIDS) was only observed in basolateral vesicles. In contrast, Cl efflux from both types of vesicles was neither substantially inhibited by DIDS nor by lowering the temperature to 0 degrees C. Phosphate efflux from basolateral membrane vesicles was found to be only partially sensitive to DIDS. Attempts to label the stilbene-sensitive SO4 pathway in basolateral vesicles using [3H2]DIDS as a marker were unsuccessful due to the nonspecific labeling of many membrane components. The asymmetry in inorganic anion transport behavior exhibited by brush border and basolateral membrane vesicles from dog renal proximal tubule was also observed in equivalent vesicles prepared from rat small intestine.

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