Glucocorticoids and metabolic acidosis-induced renal transports of inorganic phosphate, calcium, and NH4

1986 ◽  
Vol 250 (5) ◽  
pp. F827-F833 ◽  
Author(s):  
M. Boross ◽  
J. Kinsella ◽  
L. Cheng ◽  
B. Sacktor
Keyword(s):  
Metabolic Acidosis ◽  
Brush Border ◽  
Inorganic Phosphate ◽  
Brush Border Membrane ◽  
Adrenal Glands ◽  
Initial Rate ◽  
Membrane Vesicles ◽  
Ammonium Excretion ◽  
Pi Transport ◽  
Rat Proximal Tubule

The initial rate (5 s) of Na+-dependent inorganic phosphate (Pi) uptake in brush-border membrane vesicles isolated from rat proximal tubule was decreased in metabolic acidosis, 0.42 +/- 0.02 vs. 0.59 +/- 0.05 nmol/mg protein, in vesicles from control animals. Phosphate, ammonium, and Ca2+ excretions were increased 100, 600, and 56%, respectively. These changes in brush-border Pi transport and urinary excretion of ions were largely dependent on intact adrenal glands. After adrenalectomy there were no significant changes in brush-border Pi transport, Pi, and Ca2+ excretion, whereas ammonium excretion increased only 300% compared with controls. When the glucocorticoid dexamethasone was administered to adrenalectomized animals, it mimicked the effects of metabolic acidosis both in the presence and the absence of metabolic acidosis. The initial rate of brush-border Pi transport was decreased by dexamethasone administration to 0.37 +/- 0.04 nmol/mg protein in adrenalectomized acidotic animals and 0.39 +/- 0.03 nmol/mg protein in adrenalectomized animals. Dexamethasone administered to adrenalectomized acidotic animals increased Pi, ammonium, and Ca2+ excretion 190, 690, and 23%, respectively. Dexamethasone administered to nonacidotic adrenalectomized animals increased Pi ammonium and Ca2+ excretion 165, 240, and 31%, respectively. We conclude that changes in Pi, ammonium, and Ca2+ excretion observed during metabolic acidosis were dependent on intact adrenal glands and that glucocorticoids administered to adrenalectomized acidotic or nonacidotic animals mimicked the changes observed in acidotic animals with intact adrenal glands.

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.

Regulation of Na+-Pi cotransport by 1,25-dihydroxyvitamin D3 in rabbit duodenal brush-border membrane

1982 ◽  
Vol 242 (5) ◽  
pp. G533-G539 ◽  
Author(s):  
B. Hildmann ◽  
C. Storelli ◽  
G. Danisi ◽  
H. Murer
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Brush Border Membrane Vesicles ◽  
Precipitation Method ◽  
Dihydroxyvitamin D3 ◽  
1,25 Dihydroxyvitamin D3 ◽  
Pi Transport ◽  
Sodium Dependent ◽  
Cotransport System

Brush-border membrane vesicles were isolated from rabbit duodenum by a Mg2+ precipitation method, and phosphate transport was analyzed by a rapid filtration technique. Uptake of inorganic phosphate (Pi) was stimulated by an inwardly directed sodium gradient, indicating the operation of a Na-Pi cotransport system in brush-border membrane vesicles. Treatment of the animals with ethane-1-hydroxy-1,1-diphosphonate (EHDP), which is known to decrease the circulating levels of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], reduced within 3 days the sodium-dependent Pi transport in the brush-border vesicles. Injections of 1,25(OH)2D3 into rabbits increased within 9 h the sodium-dependent Pi transport in membranes from EHDP-treated animals as well as in untreated ones. The Na-D-glucose cotransport system appeared to be unaffected by these maneuvers. These results suggest that the Na-Pi cotransport system is an important site of regulation of intestinal transepithelial Pi transport by 1,25(OH)2)D3.

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.

Effect of acute acidemia on phosphate uptake by renal proximal tubular brush-border membranes

1986 ◽  
Vol 251 (5) ◽  
pp. F889-F896
Author(s):  
B. S. Levine ◽  
J. A. Kraut ◽  
D. R. Mishler ◽  
P. W. Crooks
Keyword(s):  
Metabolic Acidosis ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Respiratory Acidosis ◽  
Tissue Slices ◽  
Pi Transport ◽  
Proximal Tubular ◽  
Renal Proximal Tubular ◽  
Plasma Phosphorus

Prolonged metabolic acidosis is associated with depressed phosphate (Pi) uptake by the brush-border membrane (BBM) of the proximal tubule. To examine if changes in systemic pH underlie this inhibition, we measured Pi transport by renal cortical BBM from thyroparathyroidectomized rats with respiratory or metabolic acidosis of 1 or 3 h, respectively, and in appropriate controls. Also, Pi transport was measured in BBM prepared using tissue slices from nonacidotic rats that were preincubated for 20 or 45 min at either pH 6.9 (HCO3 = 10 mM, CO2 = 10%) or 7.4 (HCO3 = 10 mM, CO2 = 2.5%). Despite comparable acidemia (pH 7.06 +/- 0.05 with respiratory acidosis and 7.10 +/- 0.03 with metabolic acidosis), Na-dependent Pi uptake at 5 s incubation was reduced by 15.2 +/- 3.5% with respiratory acidosis compared with paired controls. It was not altered with metabolic acidosis. Vmax in respiratory acidosis (1.2 nmol X mg protein-1 X 5 s-1) was less than in controls (1.6); Kt was similar in both groups. 22Na transport and Na-dependent glucose transport were unchanged. Plasma phosphorus (P) increased from 8.75 +/- 0.35 mg/dl to 12.42 +/- 1.9 with respiratory acidosis. Therefore BBM vesicles transport was measured in controls after plasma P was raised. Under these conditions, Pi transport was similar to that with respiratory acidosis. Also Pi transport by BBM was unchanged when tissue slices were preincubated in vitro at high CO2 concentrations for 20 or 45 min. Thus respiratory acidosis specifically inhibits Na-dependent Pi transport by decreasing the number or rate of the BBM Pi carrier.(ABSTRACT TRUNCATED AT 250 WORDS)

Sulphate and phosphate transport in the renal proximal tubule

1982 ◽  
Vol 299 (1097) ◽  
pp. 549-558 ◽  
Keyword(s):  
Cell Membrane ◽  
Proximal Tubule ◽  
Brush Border ◽  
Inorganic Phosphate ◽  
Brush Border Membrane ◽  
Ph Dependence ◽  
Membrane Vesicles ◽  
Dicarboxylic Acids ◽  
Phosphate Transport ◽  
Brush Border Membrane Vesicles

Experiments performed on microperfused proximal tubules and brush-border membrane vesicles revealed that inorganic phosphate is actively reabsorbed in the proximal tubule involving a 2 Na + -HPO 2- 4 or H 2 PO 4 - co-transport step in the brush-border membrane and a sodium-independent exit step in the basolateral cell membrane. Na + - phosphate co-transport is competitively inhibited by arsenate. The transtubular transport regulation is mirrored by the brush-border transport step: it is inhibited by parathyroid hormone intracellularly mediated by cyclic AMP. Transepithelial inorganic phosphate (P i ) transport and Na + -dependent P i transport across the brush-border membrane correlates inversely with the P i content of the diet. Intraluminal acidification as well as intracellular alkalinization led to a reduction of transepithelial P i transport. Data from brush-border membrane vesicles indicate that high luminal H + concentrations reduce the affinity for Na + of the Na + -phosphate co-transport system, and that this mechanism might be responsible for the pH dependence of phosphate reabsorption. Contraluminal influx of P i from the interstitium into the cell could be partly inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS). It is not, however, changed when dicarboxylic acids are present or when the pH of the perfusate is reduced to pH 6. Sulphate is actively reabsorbed, involving electroneutral 2 Na + -SO 2 - 4 co-transport through the brush-border membrane. This transport step is inhibited by thiosulphate and molybdate, but not by phosphate or tungstate. The transtubular active sulphate reabsorption is not pH dependent, but is diminished by the absence of bicarbonate. The transport of sulphate through the contraluminal cell side is inhibited by DIDS and diminished when the capillary perfusate contains no bicarbonate or chloride. The latter data indicate the presence of an anion exchange system in the contraluminal cell membrane like that in the erythrocyte membrane.

myo-Inositol transport in renal brush border vesicles and it inhibition by D-glucose

1980 ◽  
Vol 239 (2) ◽  
pp. F113-F120 ◽  
Author(s):  
M. R. Hammerman ◽  
B. Sacktor ◽  
W. H. Daughaday
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Initial Rate ◽  
Membrane Vesicles ◽  
Electrochemical Gradient ◽  
Patients With Diabetes ◽  
Dependent Transport ◽  
The Relationship ◽  
Inositol Uptake ◽  
Renal Brush Border

We examined the mechanism of myo-inositol uptake by rabbit renal proximal tubule brush border membrane vesicles and characterized the relationship between the transports of myo-inositol and D-glucose. A 100 mM Na+ electrochemical gradient (extravesicular medium > intravesicular medium) stimulated the initial rate of myo-inositol uptake 20- to 60-fold. Other cation gradients were ineffective. The Na+ myo-inositol co-transport system was shown to be electrogenic. The Na+ electrochemical gradient-dependent uptake of myo-inositol saturated at about 1 mM myo-inositol, with an apparent Km of 94 micro M at an initial 100 mM Na+ gradient. D-Glucose was an inhibitor of the Na+ gradient-dependent uptake of myo-inositol. D-Glucose, but not L-glucose, elicited accelerative exchange diffusion of myo-inositol. myo-Inositol did not significantly inhibit the Na+ gradient-dependent transport of D-glucose. We suggest that D-glucose inhibits myo-inositol uptake by dissipating the membrane potential and sharing the myo-inositol carrier. The inhibition of myo-inositol transport across the brush border membrane by D-glucose explains how glycosuria could produce inosituria in patients with diabetes mellitus.

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