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.

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.

Pi transport, phosphorylation, and dephosphorylation in renal membranes from HYP/Y mice

1983 ◽  
Vol 245 (6) ◽  
pp. F701-F706
Author(s):  
M. R. Hammerman ◽  
L. R. Chase
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Sodium Dodecyl ◽  
Membrane Vesicles ◽  
Hypophosphatemic Rickets ◽  
Dependent Protein Kinase ◽  
Phosphoprotein Phosphatase ◽  
Pi Transport ◽  
Dependent Protein ◽  
Renal Tubular

To ascertain whether cAMP-dependent phosphorylation could be demonstrated in brush border membrane vesicles (BBMV) isolated from kidneys of mice with X-linked hypophosphatemic rickets (HYP/Y) and normal littermates (+/Y) and, if so, to determine whether the absence of dephosphorylation might underlie differences in Na+-dependent 32Pi transport in BBMV, we measured 1) 32Pi transport, 2) cAMP-dependent phosphorylation, and 3) dephosphorylation in BBMV from +/Y and HYP/Y mice. Na+ gradient-dependent 32Pi transport was decreased in BBMV from HYP/Y mice as reflected in a decreased apparent Vmax. cAMP-dependent phosphorylation of a 62,000 Mr protein was demonstrated in sodium dodecyl sulfate polyacrylamide gels of BBMV from +/Y and HYP/Y mice and was associated with decreased Na+-dependent 32Pi transport. Dephosphorylation of the 62,000 Mr band was demonstrable in both types of membranes. Thus, both cAMP-dependent protein kinase and phosphoprotein phosphatase activities were demonstrable in BBMV isolated from +/Y and HYP/Y mice. These results are consistent with the renal tubular defect in the HYP/Y mouse reflecting an intrinsic abnormality of Pi transport in the brush border membrane independent from mediation of the phosphaturic effect of parathyroid hormone.

Effect of thyroxine administration on phosphate transport across renal cortical brush border membrane

1984 ◽  
Vol 246 (2) ◽  
pp. F133-F139 ◽  
Author(s):  
R. E. Espinosa ◽  
M. J. Keller ◽  
A. N. Yusufi ◽  
T. P. Dousa
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Renal Cortex ◽  
Membrane Vesicles ◽  
Phosphate Transport ◽  
Treated Group ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular ◽  
And Control ◽  
Cortical Slices

Previous studies indicate that in hyperthyroid states the renal tubular reabsorption of phosphate is enhanced. To determine the cellular basis of this phenomenon, we investigated the effect of L-thyroxine (T4) administration on Pi transport across brush border membrane vesicles (BBMV) from rat renal cortex. Rats were thyroparathyroidectomized, fed a diet containing 1.2% phosphate, and treated intraperitoneally for 6 days with 200 micrograms T4 X 100 g body wt-1 X day-1. At the end of the treatment period, the rats had a significantly (+ delta 25%) elevated plasma Pi and a slightly decreased plasma Ca compared with controls. The renal clearance of Pi was not different between the two groups. Na+ gradient-dependent uptake of 32Pi by BBMV from renal cortex was significantly enhanced in T4-treated rats. BBMV uptake of 32Pi in the absence of Na+ -gradient as well as Na+ gradient-dependent uptake of D-[3H]glucose and L-[3H]proline did not differ between BBMV from T4-treated and control rats. Kinetic analysis showed that the Na+ gradient-dependent 32Pi transport system in BBMV from T4-treated rats had a significantly increased Vmax compared with controls (5.2 +/- 0.4 vs. 4.1 +/- 0.4 nmol Pi X 30 s-1 X mg protein-1) and also a slightly higher affinity for Pi (apparent Km in controls, 95 +/- 9; in T4-treated, 78 +/- 8 microM). Gluconeogenesis in cortical slices was not significantly different between T4-treated rats and controls. Specific activities of alkaline phosphatase and gamma-glutamyltransferase were significantly lower in BBMV from the T4-treated group compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

PTH-sensitive K(+)- and voltage-dependent Pi transport by chick renal brush-border membranes

1993 ◽  
Vol 265 (6) ◽  
pp. F822-F829 ◽  
Author(s):  
L. E. Barber ◽  
V. Coric ◽  
N. B. Clark ◽  
J. L. Renfro
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Pi Transport ◽  
Positive Voltage ◽  
Carbonyl Cyanide ◽  
Renal Brush Border Membranes ◽  
Voltage Dependent ◽  
Renal Tubular ◽  
Dependent Transport

Brush-border membrane vesicles (BBMV) from chick (Gallus gallus) kidneys were used to examine possible pathways of Pi transport associated with Pi secretion. Preloading with 6 mM Pi trans-stimulated 32Pi uptake in the absence of Na+, indicating facilitation. Inside-positive voltage (100 mM K+, out > in, +valinomycin) increased Pi uptake from 161 +/- 4.4 to 241 +/- 16.1 pmol.mg protein-1.5s-1 at pH 7.5 (in = out). Gradients characterized by extravesicular pH (pHo) of 5.5 vs. intravesicular pH (pHi) of 7.5, 100 mM K+ (out > in), without and with valinomycin, further increased uptake to 664 +/- 148.5 and 946 +/- 90.8 pmol.mg protein-1.5s-1, respectively. Carbonyl cyanide m-chlorophenylhydrazone (CCCP) had no effect on the latter response, but with 100 mM K+ (in = out), valinomycin decreased the response more than one-half, implicating a H+ diffusion potential. Generation of this potential with pHo 5.5 vs. pHi 7.5 and CCCP did not drive concentrative Pi uptake in absence of K+. Parathyroid hormone (PTH) treatment significantly increased this BBMV K(+)- and voltage-dependent Pi up-take compared with the parathyroidectomized (PTX) condition. The values of maximal uptake rate (Vmax) in PTH vs. PTX BBMV were 5,330 and 1,976 pmol.mg protein-1.5s-1, respectively. K(+)-dependent transport was inhibited by arsenate, phosphonoacetic acid, and vanadate. Together, the data indicate that this PTH-sensitive, voltage- and K(+)-dependent monovalent Pi transporter could be the mechanism by which Pi exits, cell-to-lumen, during renal tubular Pi secretion.

Ureteral occlusion decreases phospholipid and cholesterol of renal tubular membranes

1986 ◽  
Vol 250 (1) ◽  
pp. F136-F143
Author(s):  
J. Morrissey ◽  
D. Windus ◽  
S. Schwab ◽  
J. Tannenbaum ◽  
S. Klahr
Keyword(s):  
Ureteral Obstruction ◽  
Unilateral Ureteral Obstruction ◽  
Phospholipid Content ◽  
Contralateral Kidney ◽  
Basolateral Membranes ◽  
Renal Tubular Cells ◽  
Altered Response ◽  
Renal Tubular ◽  
Tubular Membranes ◽  
Ureteral Occlusion

Unilateral ureteral obstruction of 24 h duration in the dog results in a 20% decrease in the amount of total phospholipids present in basolateral membranes of renal tubular cells obtained from the experimental kidney as compared with the amount of phospholipid in basolateral membranes prepared from the contralateral kidney of the same dogs or from the kidneys of normal sham-operated dogs. There was also a decrease in the content of cholesterol and cholesterol esters of the basolateral membranes from the experimental kidney. By contrast, no significant change in lipid content was observed in brush border membranes obtained from the experimental kidney of dogs with unilateral ureteral obstruction. The decrease in phospholipid content of basolateral membranes was accompanied by a 40% fall in the content of phosphatidylcholine and a 12% fall in sphingomyelin. There was a small (12%) but significant increase in the content of phosphatidylethanolamine in basolateral membranes. The mechanisms responsible for the selective decrease in phospholipid content of basolateral membranes remain to be established. It is postulated that changes in solute transport and altered response to hormones observed in the postobstructed kidney of animals with unilateral ureteral obstruction may be explained, at least in part, by changes in the lipid composition of basolateral membranes.

Potential differences influence amino acid/Na+ symport rates in larval Manduca sexta midgut brush-border membrane vesicles.

1994 ◽  
Vol 189 (1) ◽  
pp. 55-67
Author(s):  
R Parthasarathy ◽  
W R Harvey
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Manduca Sexta ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Brush Border Membrane Vesicles ◽  
Rate Determining Step ◽  
Half Saturation Constant

The time-dependent fluorescence intensity of an intravesicular potential-sensitive dye was used to probe the real-time kinetics of potential difference (PD)-dependent amino acid/Na+ symport at pH9 into brush-border membrane vesicles obtained from larval Manduca sexta midgut. Neutral amino acids (alanine, proline) are symported at higher rates as the vesicles are hyperpolarized. The symport rates of acidic (glutamate) and basic (arginine) amino acids are almost PD-independent. The half-saturation constant of alanine is PD-independent between -108 and -78 mV, although the maximal symport velocity increases by half as the voltage is increased. Amino acid throughput is evidently enhanced as the relatively high transmembrane PDs (> 150 mV, lumen positive) measured in vivo are approached. The half-saturation concentrations of Na+ were in the range 15-40 mmol l-1 for most of the amino acids examined and increased with voltage for alanine. The Vmax observed as a function of cation or amino acid concentration increased as the vesicle was hyperpolarized in the case of leucine and alanine. The data support the hypothesis that carrier and substrates are at equilibrium inasmuch as substrate translocation seems to be the rate-determining step of symport.

scholarly journals Role of Sirolimus in renal tubular apoptosis in response to unilateral ureteral obstruction

2018 ◽  
Vol 15 (13) ◽  
pp. 1433-1442 ◽  
Author(s):  
Mei Yang ◽  
Yang-yang Zhuang ◽  
Wei-wei Wang ◽  
Hai-ping Zhu ◽  
Yan-jie Zhang ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Unilateral Ureteral Obstruction ◽  
Renal Tubular

Recovery from Acute Ischaemic Renal Failure is Accelerated by Des-(1–3)-Insulin-Like Growth Factor-1

1994 ◽  
Vol 86 (6) ◽  
pp. 709-714 ◽  
Author(s):  
Ross Clark ◽  
Deborah Mortensen ◽  
Ralph Rabkin
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Growth Factor ◽  
Fractional Excretion ◽  
Insulin Like Growth Factor ◽  
Ischaemic Injury ◽  
Beneficial Effects ◽  
Nitrogen Levels ◽  
Renal Tubular Cells ◽  
Renal Tubular

1. Acute renal failure carries a high risk of morbidity and mortality, so there is a need for agents that minimize renal injury after an insult and that hasten repair. Insulin-like growth factor-1 is mitogenic for renal tubular cells; in normal kidneys it has haemodynamic effects and it is potently anabolic. We tested the theory that insulin-like growth factor-1 may be of use in the treatment of acute renal failure by administering recombinant des-(1–3)-insulin-like growth factor-1, a truncated form of insulin-like growth factor-1, which occurs naturally. Ischaemic renal failure was induced in normal rats by occluding both renal pedicles for 60 min. Then des-(1–3)-insulin-like growth factor-1 (0.8 mg day−1 kg−1) or vehicle was given by subcutaneous minipump for 7 days. The rats were weighed and bled daily and in one experiment were housed in metabolic cages and urine was collected. 2. Des-(1–3)-insulin-like growth factor-1 caused a lower and earlier peak in both serum creatinine and blood urea-nitrogen levels, and a more rapid and complete return toward basal values than in untreated animals. Also des-(1–3)-insulin-like growth factor-1 significantly increased creatinine clearance and reduced fractional excretion of filtered sodium. Besides these beneficial effects on kidney function, des-(1–3)-insulin-like growth factor-1 was anabolic as treated rats gained weight while control rats lost weight. The mortality in control rats was 28% compared with 6% in treated rats. 3. Thus des-(1–3)-insulin-like growth factor-1 accelerated recovery from acute ischaemic injury and may be useful for the treatment of acute renal failure.

Urate transport in the proximal tubule: in vivo and vesicle studies

1985 ◽  
Vol 249 (6) ◽  
pp. F789-F798 ◽  
Author(s):  
A. M. Kahn ◽  
E. J. Weinman
Keyword(s):  
Proximal Tubule ◽  
Brush Border ◽  
Anion Exchanger ◽  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Transport Processes ◽  
Basolateral Membrane Vesicles ◽  
Urate Transport ◽  
Rat Proximal Tubule

The transport of urate in the mammalian nephron is largely confined to the proximal tubule. Depending on the species, net reabsorption or net secretion is observed. The rat, like the human and the mongrel dog, demonstrates net reabsorption of urate and has been the most extensively studied species. The unidirectional reabsorption and secretion of urate in the rat proximal tubule occur via a passive and presumably paracellular route and by a mediated transcellular route. The reabsorption of urate, and possibly its secretion, can occur against an electrochemical gradient. A variety of drugs and other compounds affect the reabsorption and secretion of urate. The effects of these agents depend on their site of application (luminal or blood), concentration, and occasionally their participation in transport processes that do not have affinity for urate. Recent studies with renal brush border and basolateral membrane vesicles from the rat and brush border vesicles from the dog have determined the mechanisms for urate transport across the luminal and antiluminal membranes of the proximal tubule cell. Brush border membrane vesicles contain an anion exchanger with affinity for urate, hydroxyl ion, bicarbonate, chloride, lactate, p-aminohippurate (PAH), and a variety of other organic anions. Basolateral membrane vesicles contain an anion exchanger with affinity for urate and chloride but not for PAH. Both membrane vesicle preparations also permit urate translocation by simple diffusion. A model for the transcellular reabsorption and secretion of urate in the rat proximal tubule is proposed. This model is based on the vesicle studies, and it can potentially explain the majority of urate transport data obtained with in vivo techniques.

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