Renal adaptation to dietary phosphate deprivation: role of proximal tubule brush-border membrane fluidity

1991 ◽  
Vol 260 (5) ◽  
pp. F613-F618 ◽  
Author(s):  
B. S. Levine ◽  
K. A. Knibloe ◽  
K. Golchini ◽  
S. Hashimoto ◽  
I. Kurtz
Keyword(s):  
Proximal Tubule ◽  
Brush Border ◽  
Temporal Relationship ◽  
Brush Border Membrane ◽  
Renal Cortex ◽  
Pi Transport ◽  
Renal Adaptation ◽  
Dietary Phosphate ◽  
Pi Deprivation

With dietary phosphate (Pi) restriction, fluidity of renal proximal tubule brush-border membranes (BBM) and Na-dependent Pi transport (Na-Pi) are increased, suggesting that changes in BBM fluidity are critical for adaptation to Pi restriction. To test this hypothesis, the temporal relationship between Na-Pi transport and changes in BBM fluidity was assessed after Pi deprivation in rats. Renal cortex was obtained from rats fed either a 0.03% (-P) or a 0.6% (+P) Pi diet for 4 h or 7 days, and BBM were prepared. Na-Pi uptake by BBM was measured by use of rapid filtration, and BBM fluidity was assessed by use of the fluorescent probe 1,6-diphenyl-1,3,5-hexatriene (DPH). After 4 h on the diets, Na-Pi uptake was 439 +/- 142 (SD) and 984 +/- 184 pmol.mg protein-1.5 s-1 in +P and -P, respectively (P less than 0.01, n, = 8). Na-dependent proline uptake was unchanged. DPH anisotropy and total cholesterol were similar between groups: 0.204 +/- 0.025 and 0.401 +/- 0.047 nmol/mg protein, respectively, in +P and 0.205 +/- 0.015 and 0.392 +/- 0.037 in -P (P greater than 0.05, n = 8-10). After 7 days, Na-Pi uptake was 841 +/- 291 in +P and 2,168 +/- 848 pmol.mg protein-1.5 s-1 in -P, P less than 0.01, n = 8. DPH anisotropy and BBM cholesterol were 0.175 +/- 0.019 and 443 +/- 132 nmol/mg protein, respectively, in +P and 0.162 +/- 0.020 (n = 8) and 341 +/- 128 (n = 3) in -P (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin stimulates Pi transport in brush border vesicles from proximal tubular segments

1984 ◽  
Vol 247 (5) ◽  
pp. E616-E624 ◽  
Author(s):  
M. R. Hammerman ◽  
S. Rogers ◽  
V. A. Hansen ◽  
J. R. Gavin
Keyword(s):  
Proximal Tubule ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Direct Action ◽  
Membrane Vesicles ◽  
Pi Transport ◽  
Glomerular Filtrate ◽  
Dog Kidney ◽  
Proximal Tubular ◽  
Altered Transport

Induction of hyperinsulinemia in dogs results in enhanced reabsorption of Pi from glomerular filtrate in the renal proximal tubule. To determine whether this may be a direct action of insulin mediated by altered transport characteristics of the proximal tubular brush border membrane, we measured Na+-dependent 32Pi transport in brush border membrane vesicles prepared from isolated proximal tubular segments originating from dog kidney that had been incubated with or without insulin. Specific high affinity binding sites for insulin were detected in proximal tubular segments. Increased initial rates (15 s) of Na+-dependent 32Pi transport were measured in brush border vesicles prepared from segments that had been incubated with insulin. This effect of insulin was concentration dependent over the range of 10(-10) to 10(-6) M insulin. These studies demonstrate the feasibility of using brush border vesicles prepared from proximal tubular segments to study solute transport. Our findings suggest that insulin-induced increased Pi reabsorption in the proximal tubule is mediated by a direct action of insulin on the proximal tubular cell, which results in increased Na+-Pi cotransport across the brush border membrane.

scholarly journals Effect of dietary phosphate intake on phosphate transport by isolated rat renal brush-border vesicles

1979 ◽  
Vol 180 (3) ◽  
pp. 465-470 ◽  
Author(s):  
Reinhard Stoll ◽  
Rolf Kinne ◽  
Heini Murer
Keyword(s):  
Proximal Tubule ◽  
Brush Border ◽  
Dry Matter ◽  
Brush Border Membrane ◽  
Phosphate Uptake ◽  
Membrane Vesicles ◽  
Phosphate Transport ◽  
Phosphate Intake ◽  
Dietary Phosphate ◽  
Renal Brush Border

Renal brush-border membrane vesicles isolated from rats kept for 6–8 weeks on a low-phosphate diet (0.15% of dry matter) showed a markedly faster Na+-dependent phosphate uptake than did membrane vesicles isolated from animals kept on a high-phosphate diet (2% of dry matter). Phosphate-uptake rate by brush-border membrane vesicles isolated from animals on a low-phosphate diet remained significantly increased after acute parathyroidectomy. Dietary adaptation was also observed in animals that had been parathyroidectomized before exposure to the different diets. In animals on the low-phosphate diet parathyrin administration inhibited phosphate uptake by brush-border vesicles only if the animals were repleted with Pi (5ml of 20mm-NaH2PO4) 1h before being killed. After acute phosphate loading and parathyrin administration the difference in the transport rate between the two dietary groups remained statistically significant. The results suggest that the adaptation of proximal-tubule phosphate transport to dietary intake of phosphate is reflected in the Na+/phosphate co-transport system located in the luminal membrane of the proximal-tubule cell. Since the dietary effects on phosphate transport by brush-border membranes are only partially reversed by acute changes in parathyrin concentration and are also observed in chronically parathyroidectomized animals, the adaptation of the Na+/phosphate co-transport system to dietary phosphate intake seems to involve an additional mechanism independent of parathyrin.

Renal adaptation to low-phosphate diet in diabetic rats

1992 ◽  
Vol 262 (5) ◽  
pp. F731-F736 ◽  
Author(s):  
M. I. Abraham ◽  
R. E. Woods ◽  
D. K. Breedlove ◽  
S. A. Kempson
Keyword(s):  
Proximal Tubule ◽  
Adaptive Response ◽  
Plasma Insulin ◽  
Brush Border Membrane ◽  
Diabetic Rats ◽  
Compensatory Response ◽  
Pi Transport ◽  
Renal Adaptation ◽  
Streptozotocin Induced Diabetes ◽  
Cotransport System

Insulin stimulates the Na(+)-Pi cotransport system in the brush-border membrane (BBM) of the renal proximal tubule, and an acute decrease in plasma insulin leads to a decrease in renal reabsorption of Pi. It has been proposed that insulin may play a role in the rapid renal adaptation to dietary deprivation of Pi. This hypothesis was tested using rats with low plasma insulin due to streptozotocin-induced diabetes. Both control and diabetic rats were housed in metabolic cages and fed either a normal Pi diet or a low Pi diet for 3 days. At the end of the third day, BBM vesicles were prepared from renal cortex and Na(+)-Pi cotransport was measured. At the whole kidney level, diabetic rats showed a normal adaptive response. There was a prompt and marked decrease in urinary Pi excretion when the rats ate a low Pi diet. At the BBM level, however, the adaptive response was absent. There was no increase in Na(+)-Pi cotransport in diabetic rats fed low Pi diet. Treatment of diabetic rats with exogenous insulin before feeding low Pi diet restored the adaptive increase in Pi transport by BBM. Insulin appears to be required for the adaptation of proximal tubule Pi transport to low Pi diet. In the absence of this adaptation in proximal tubule BBM, a compensatory response in the kidney may produce an increase in Pi reabsorption in later segments of the nephron.

Renal adaptation to phosphate deprivation in the Hyp mouse with X-linked hypophosphatemia

1979 ◽  
Vol 57 (6) ◽  
pp. 938-944 ◽  
Author(s):  
H. S. Tenenhouse ◽  
C. R. Scriver
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Control Diet ◽  
Fractional Excretion ◽  
Kidney Cortex ◽  
Phosphate Deprivation ◽  
Renal Adaptation ◽  
Pi Deprivation

The mechanism of renal adaptation to variation in dietary inorganic phosphate (Pi) was investigated in intact Hyp/+ (heterozygous) mice and +/+ (normal homozygous) female siblings. Hyp/+ mice were selected for expression of the X-linked Hyp allele, when fed the control diet (0.6% P), by evidence of persistent postweaning hypophosphatemia (1.78 ± 0.08 mM, mean ± SE, versus 2.68 ± 0.19 mM in +/+ siblings (p < 0.01)). Hyp/+ mice had an elevated fractional excretion index for Pi (FEIPi) (0.570 ± 0.024, mean ± SE) on this diet versus +/+ siblings (0.352 ± 0.025, p < 0.001). Renal cortex content of Pi (~46 nmol/mg protein) and net radioisotopic uptake of Pi by slices were similar in Hyp/+ and +/+ mice. Purified brush border membrane vesicles (BBMV) from Hyp/+ kidney cortex transported labelled Pi (100 μM) by a Na+-dependent mode at about one-half the rate (p < 0.001) observed in +/+ mice. Hyp/+ and +/+ mice fed a low P diet (0.03%) maintained their phenotypic differences in vivo and in vitro. Both adapted to chronic (> 2 week) Pi deprivation with a striking reduction (40- to 50-fold) of FEIPi (p < 0.001) and a fall in plasma [Pi] (p < 0.001). Neither the renal Pi content nor uptake of Pi by slices changed in deprived Hyp/+ and +/+ mice. On the other hand, BBMV uptake by Na+-dependent cotransport increased 200% (p < 0.001) during Pi deprivation in both the Hyp/+ and +/+ mouse. D-glucose transport did not increase. We conclude that renal adaptation to phosphate deprivation is achieved by modulation of a component of Na+-dependent cotransport in brush border membrane that is not controlled by the X-linked gene.

Effect of luminal angiotensin II on proximal tubule fluid transport: role of apical phospholipase A2

1994 ◽  
Vol 266 (2) ◽  
pp. F202-F209 ◽  
Author(s):  
L. Li ◽  
Y. P. Wang ◽  
A. W. Capparelli ◽  
O. D. Jo ◽  
N. Yanagawa
Keyword(s):  
Angiotensin Ii ◽  
Phospholipase A2 ◽  
Proximal Tubule ◽  
Brush Border ◽  
Fluid Transport ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Ang Ii ◽  
Potent Effect

Recent micropuncture studies showed the existence of high concentrations of angiotensin II (ANG II) in proximal tubular fluid. In the present study, we have examined the effect of luminal ANG II, alone and in combination with peritubular ANG II, on fluid transport (JV) in the isolated perfused rabbit proximal convoluted tubule. In comparison with peritubular ANG II, luminal ANG II caused a similar but more potent biphasic effect on JV. At 10(-11) M, luminal ANG II maximally increased JV to 204 +/- 22% of the baseline compared with 142 +/- 10% by peritubular ANG II at 10(-10) M. At 10(-8) M, luminal ANG II suppressed JV to 9.7 +/- 16% of the baseline compared with 64 +/- 14% by peritubular ANG II. When luminal and peritubular ANG II were combined at concentrations that impose similar effect on JV, the effects of luminal and peritubular ANG II were not additive. However, when combined at concentrations that would otherwise impose opposing effects on JV, the stimulatory effect predominated. In support of the role of apical phospholipase A2 (PLA2) on the effect of luminal ANG II, ANG II stimulated PLA2 activity in isolated brush-border membrane vesicles, and addition of PLA2 inhibitor, mepacrine or dibucaine, to the luminal perfusate attenuated the effect of luminal ANG II on JV. In summary, these studies show a potent effect of luminal ANG II on proximal tubule JV involving activation of brush-border membrane PLA2. When combined, luminal and peritubular ANG II exert their effects in concert on proximal tubule JV.

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