Interrelations of arsenate and phosphate transport in the dog kidney

1963 ◽  
Vol 205 (4) ◽  
pp. 707-714 ◽  
Author(s):  
J. M. Ginsburg ◽  
W. D. Lotspeich

The relation between arsenate and phosphate transport in the dog kidney was studied by measuring the renal clearance of arsenate labeled with its radioactive isotope As74. The experiments were performed during osmotic diuresis induced by mannitol. The results demonstrate certain similarities in the transport of these ions. Arsenate undergoes a net tubular reabsorption which is inhibited as the plasma phosphate concentration is raised. The inverse relationship between arsenate transport and the plasma As:P ratio suggests a competitive mechanism for the interaction between the two ions Like phosphate, arsenate transport is inhibited by glucose and this effect is reversed by phlorizin. An important difference between arsenate and phosphate transport is the sensitivity of arsenate transport to urine flow. In vivo reduction of arsenate to arsenite and a net tubular secretion of arsenite has been observed. The results are discussed in terms of the known ability of arsenate to substitute for phosphate in biochemical reactions.

1964 ◽  
Vol 207 (1) ◽  
pp. 113-117 ◽  
Author(s):  
Gabrielle H. Reem ◽  
Parker Vanamee

Sodium lactate was infused and urate clearance was measured under conditions of osmotic diuresis alone, as well as during simultaneous urate infusion. Urate clearance in the Dalmatian was not depressed by the administration of sodium lactate of 1.2–9.3 mEq/kg dl-sodium lactate, indicating that sodium lactate has no inhibitory effect on tubular secretion of urate. dl-Sodium lactate, 0.54–11.8 mEq/kg, was administered to four mongrel dogs in five experiments. In three experiments a significant drop of urate clearance in relation to filtration rate was observed. In two experiments in which urine flows exceeded 10 ml/min no significant decrease in urate clearance was recorded following dl-sodium lactate administration. The depression of urate clearance in the mongrel under conditions of moderate urine flow where reabsorption of solutes is more easily accomplished, and the absence of this effect in the Dalmatian as well as in the mongrel under conditions of vigorous diuresis where reabsorption of solutes is greatly diminished, lends support to the belief that sodium lactate depresses urate clearance by facilitating urate reabsorption in the mongrel.


1962 ◽  
Vol 203 (6) ◽  
pp. 975-979 ◽  
Author(s):  
Stephen S. Chan ◽  
William D. Lotspeich

The net tubular reabsorption of glucose (TG) was measured simultaneously in both kidneys of the cat before, during, and after the infusion of small amounts of phlorizin and phloretin at constant rates into one renal artery. Experiments were performed at endogenous and elevated blood glucose levels. The results show that phlorizin blocks glucose transport across the renal tubule at concentrations in renal blood and tissue in the range of 10–5 to 10–7 m. These estimates agree with those for dog kidney in vivo and hamster small intestine in vitro. In addition to this high affinity of phlorizin for the tubular glucose carrier, the experiments also reveal the easily dissociable nature of the phlorizin carrier complex. When blood glucose is elevated the TG is even more sensitive to small concentrations of phlorizin. At all blood glucose levels the aglucone, phloretin, is at least ten times less effective in inhibiting TG than phlorizin itself. These findings are discussed in relation to critical groupings in the phlorizin molecule.


1977 ◽  
Vol 232 (3) ◽  
pp. F235-F238 ◽  
Author(s):  
R. F. Greger ◽  
F. C. Lang ◽  
F. G. Knox ◽  
C. P. Lechene

The presence of phosphate secretion by the renal tubule in mammals has been controversial. Recently, in a micropuncture and microperfusion study, net secretion of phosphate was reported for the proximal tubule of rats which were infused with parathyroid hormone (PTH) and phosphate. Since the finding of net secretion of phosphate by the proximal tubule is in contradiction to other reports, the question was reinvestigated with the use of microperfusion techniques that were modified to allow identification of sample contamination. Studies were performed in intact dogs, phosphate- and PTH-loaded intact rats, and phosphate-loaded, acutely thyroparathyroidectomized rats. After exclusion of contaminated samples, no significant influx of phosphate was found in any of the three groups. Neither increased plasma phosphate concentration nor the infusion of parathyroid hormone unmasked a secretory process for phosphate. It is concluded that phosphate transport in the proximal tubule is essentially a unidirectional phenomenon, i.e., reabsorption is not opposed by significant backflux of phosphate.


1982 ◽  
Vol 243 (5) ◽  
pp. F471-F475 ◽  
Author(s):  
A. Hoppe ◽  
M. Metler ◽  
T. J. Berndt ◽  
F. G. Knox ◽  
S. Angielski

Respiratory alkalosis induced hypophosphatemia and hypophosphaturia in intact animals. The present studies evaluated the effect of respiratory alkalosis on tissue phosphate distribution and renal phosphate transport in the presence and absence of parathyroid hormone (PTH). Respiratory alkalosis decreased plasma phosphate concentration and increased phosphate concentrations in muscle and liver. It decreased fractional phosphate excretion (FEPi) from 6.1 +/- 1.4 to 0.6 +/- 0.2%. In thyroparathyroidectomized (TPTX) rats infused with 20 mM phosphate, respiratory alkalosis decreased FEPi from 15.0 +/- 0.9 to 5.5 +/- 0.1%. PTH or dibutyryl cAMP administration produced a phosphaturia that was blunted by respiratory alkalosis. The phosphaturic response to PTH was also blunted in hypocapnic rats in which alkalosis was prevented by infusion of HCl. We conclude that respiratory alkalosis increases phosphate uptake by muscle, which largely accounts for the hypophosphatemia. The kidney response with increased phosphate reabsorption independent of plasma and kidney phosphate concentrations and with refractoriness to the phosphaturic effect of PTH. This refractoriness to the phosphaturic effect of PTH is due to decreased PCO2 rather than to the concomitant extracellular alkalosis.


1977 ◽  
Vol 233 (2) ◽  
pp. F138-F144 ◽  
Author(s):  
N. B. Clark ◽  
R. F. Wideman

Renal excretion patterns of calcium, phosphate, sodium, and potassium were studied in parathyroidectomized (PTX) and parathyroid extract (PTE)-injected PTX starlings. Sturnus vulgaris. Anesthetized birds (Equi-Thesin or Dial) were infused intravenously with 2.5% mannitol containing [14C]inulin. PTX caused significant hypocalcemia, hyperphosphatemia, increased relative calcium clearance (CCa/CIn), and decreased relative clearances of phosphate and potassium, but did not change the clearance of sodium. Glomerular filtration rate (GFR=CIn) and urine flow remained unchanged up to 2 h after PTX. PTE administration 3 h after PTX returned serum calcium and phosphate values to control levels and caused a transient (10-min) increase in GFR. Following PTE, the relative clearances of phosphate, sodium- and potassium increased, while that of calcium decreased significantly relative to the PTX levels. PTE caused net tubular secretion of phosphate, decreased tubular reabsorption of sodium and potassium (sometimes potassium secretion), and a return of excretion of calcium to control levels. These studies indicate that the parathyroid role in calcium and phosphate homeostasis in starlings is predominantly on the kidney.


1958 ◽  
Vol 196 (1) ◽  
pp. 93-99 ◽  
Author(s):  
Julius J. Cohen ◽  
Marcus A. Krupp ◽  
Charles A. Chidsey ◽  
Charles I. Biltz

In renal clearance experiments with dogfish, trimethylamine HCL (TMA) administration (i.m.) results in a large increase in trimethylamine oxide (Oxide) excretion. This is shown to occur by inhibition of net renal tubular reabsorption of the Oxide. The TMA, on the other hand, reaches the urine by net tubular secretion in quantities which are consistent with the attainment of diffusion equilibrium across the pH gradient between urine and plasma. The effect of TMA is not related to increased urine flow but is a specific effect on Oxide reabsorption. The administration of the homologue of TMA, dimethylamine, results in a similar but less profound blockade of Oxide reabsorption. Methylamine, however, has no effect at all on Oxide reabsorption. Large excretory losses of TMAO occurred without any change in TMAO plasma level, further indicating the physiological regulation of the plasma concentration of this weak base.


1959 ◽  
Vol 197 (3) ◽  
pp. 580-584 ◽  
Author(s):  
Mary F. Paul ◽  
Raymond C. Bender ◽  
Esther G. Nohle

Renal clearance of nitrofurantoin at various plasma levels was determined in the white rat. The clearance ratios (nitrofurantoin/inulin) exhibited a curvilinear relationship with the plasma level of the drug. The excretion of nitrofurantoin was found to be dependent upon the three following factors: glomerular filtration, tubular secretion and tubular reabsorption. The clearance of nitrofurantoin was not affected by urine flow nor by concurrent PAH administration. It was increased by acetazolamide and decreased slightly by probenecid. Thirty to forty per cent of the dose was recovered in the urine of rats or dogs after either per oral or intravenous administration. Rapid distribution of the drug was indicated by low plasma concentrations following intravenous administration.


1984 ◽  
Vol 246 (3) ◽  
pp. F323-F333 ◽  
Author(s):  
G. A. Quamme ◽  
N. L. Wong

The effect of intraluminal hydrogen ion concentration on phosphate absorption was evaluated in the rat superficial proximal tubule. Early proximal convoluted tubules were perfused in vivo with buffered equilibrium solutions, and the saturation kinetics for phosphate transport was determined by altering intraluminal phosphate concentration at pH values of 7.65 and 6.5. The apparent Jmax and Km parameters of phosphate transport were about twofold greater with intraluminal pH 7.65 compared with pH 6.5 values. Accordingly, intraluminal hydrogen ion had a direct effect on tubular phosphate transport. Endogenous or exogenously administered parathyroid hormone inhibited phosphate absorption at both pH values, indicating that the phosphaturic action of parathyroid hormone is independent of the intraluminal pH value. Elevation of plasma phosphate inhibited phosphate absorption unrelated to the intraluminal phosphate concentration at both pH values. These data suggest that elevation of plasma phosphate may decrease phosphate absorption by inhibiting efflux from the cell into the peritubular capillary. In conclusion, proximal phosphate absorption is determined by the intraluminal pH value, circulating parathyroid hormone level, and plasma phosphate concentration acting through separate cellular and membrane mechanisms.


2000 ◽  
Vol 279 (4) ◽  
pp. R1268-R1276 ◽  
Author(s):  
Paul P. Leyssac ◽  
Niels-Henrik Holstein-Rathlou ◽  
Ole Skøtt

Inconsistencies in previous reports regarding changes in early distal NaCl concentration (EDNaCl) and renin secretion during osmotic diuresis motivated our reinvestigation. After intravenous infusion of 10% mannitol, EDNaCl fell from 42.6 to 34.2 mM. Proximal tubular pressure increased by 12.6 mmHg. Urine flow increased 10-fold, and sodium excretion increased by 177%. Plasma renin concentration (PRC) increased by 58%. Renal blood flow and glomerular filtration rate decreased, however end-proximal flow remained unchanged. After a similar volume of hypotonic glucose (152 mM), EDNaClincreased by 3.6 mM, ( P < 0.01) without changes in renal hemodynamics, urine flow, sodium excretion rate, or PRC. Infusion of 300 μmol NaCl in a smaller volume caused EDNaCl to increase by 6.4 mM without significant changes in PRC. Urine flow and sodium excretion increased significantly. There was a significant inverse relationship between superficial nephron EDNaCl and PRC. We conclude that EDNa decreases during osmotic diuresis, suggesting that the increase in PRC was mediated by the macula densa. The results suggest that the natriuresis during osmotic diuresis is a result of impaired sodium reabsorption in distal tubules and collecting ducts.


1980 ◽  
Vol 238 (1) ◽  
pp. F31-F36 ◽  
Author(s):  
J. P. Johnson ◽  
S. Green ◽  
J. H. Schwartz

The effects of changes in pH and addition of CO2/HCO3- on transepithelial phosphate transport were studied in turtle urinary bladder. Net mucosa-to-serosa flux of phosphate (JP) was determined as the difference between unidirectional 32P fluxes in the absence of transepithelial electrochemical gradients. With 5 mM phosphate in HCO3--free Ringer at pH 8.4, JP was 21.8 +/- 7.4 nmol . 8 cm-2 . h-1. There was a slight increase in JP with isohydric addition of 10 mM HCO3-. Addition of 5% CO2, which reduced pH to 7.3, did not affect JP. At pH 8.4, JP was not affected by ouabain or dinitrophenol and increased progressively as phosphate concentration was raised between 0.5 and 10 mM. At pH 6.2 in the absence of exogenous CO2 and HCO3-, JP was undectable. With 2.5 mM HCO3- and 5% CO2 at pH 6.5, JP was 61.3 +/- 16.0 and decreased to 30.6 +/- 1.6 nmol . 8 cm-2 . h-1 when pH was raised to 7.2 by increasing HCO3- to 10 mM. At pH 6.5 JP was inhibited by both ouabain and dinitrophenol. These results suggest that at acidic pH, JP results from the tranport of H2PO4-. The transport of H2PO4- is CO2 dependent and inhibited by ouabain and dinitrophenol. In contrast, at alkaline pH, JP results from the transport of HPO4(2-), which is neither CO2 dependent nor inhibited by ouabain or dinitrophenol.


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