SOME EFFECTS OF PHLORIZIN AND PHLORETIN ON RENAL AMINO ACID REABSORPTION IN THE DOG

1965 ◽  
Vol 43 (1) ◽  
pp. 79-87 ◽  
Author(s):  
William A. Webber

The effects of phlorizin and phloretin on amino acid reabsorption were studied using clearance techniques in dogs. At endogenous plasma amino acid concentrations no effects were demonstrable. At elevated amino acid levels phlorizin depressed the reabsorption of L-aspartic acid and L-lysine. Phloretin depressed the reabsorption of L-aspartic acid but had a slight enhancing effect on that of L-lysine. No definite effects were observed on L-alanine or glycine reabsorption. These results are not predictable from the observations of other workers that in the in vitro rat kidney cortex phlorizin increases amino acid concentrating ability while phloretin depresses it. Our results are not, however, incompatible with the in vitro observations since it is theoretically possible for an agent to enhance the concentrating ability of kidney cortex, and either depress or increase tubular reabsorption, depending on whether the predominant site of action is on the luminal or basal side of the proximal tubular cells.

1967 ◽  
Vol 45 (5) ◽  
pp. 867-872 ◽  
Author(s):  
William A. Webber

Amino acid excretion patterns were studied in rats 2 to 12 weeks old. In general there was a decline in amino acid excretion over this period which paralleled that reported in human infants by other workers. The decrease was most marked for certain amino acids (glycine, histidine, and arginine). These changes in excretion are not explicable in terms of changes in plasma amino acid concentrations, nor is it likely that they result from differences in filtered load. They may reflect a progressive development of transport mechanisms for some amino acids over the period studied, in which case similar changes in the concentrating ability of rat kidney cortex slices would be predicted. Other possible explanations which are less readily tested include changes in permeability of the tubular cell membranes and differences in the glomerular filtering capacity relative to the amount of tubular tissue which has developed.


2003 ◽  
Vol 285 (3) ◽  
pp. C608-C617 ◽  
Author(s):  
Snezana Petrovic ◽  
Liyun Ma ◽  
Zhaohui Wang ◽  
Manoocher Soleimani

SLC26A6 (or putative anion transporter 1, PAT1) is located on the apical membrane of mouse kidney proximal tubule and mediates [Formula: see text] exchange in in vitro expression systems. We hypothesized that PAT1 along with a [Formula: see text] exchange is present in apical membranes of rat kidney proximal tubules. Northern hybridizations indicated the exclusive expression of SLC26A6 (PAT1 or CFEX) in rat kidney cortex, and immunocytochemical staining localized SLC26A6 on the apical membrane of proximal tubules, with complete prevention of the labeling with the preadsorbed serum. To examine the functional presence of apical [Formula: see text] exchanger, proximal tubules were isolated, microperfused, loaded with the pH-sensitive dye BCPCF-AM, and examined by digital ratiometric imaging. The pH of the perfusate and bath was kept at 7.4. Buffering capacity was measured, and transport rates were calculated as equivalent base flux. The results showed that in the presence of basolateral DIDS (to inhibit [Formula: see text] cotransporter 1) and apical EIPA (to inhibit Na+/H+ exchanger 3), the magnitude of cell acidification in response to addition of luminal Cl– was ∼5.0-fold higher in the presence than in the absence of [Formula: see text]. The Cl–-dependent base transport was inhibited by ∼61% in the presence of 0.5 mM luminal DIDS. The presence of physiological concentrations of oxalate in the lumen (200 μM) did not affect the [Formula: see text] exchange activity. These results are consistent with the presence of SLC26A6 (PAT1) and [Formula: see text] exchanger activity in the apical membrane of rat kidney proximal tubule. We propose that SLC26A6 is likely responsible for the apical [Formula: see text] (and Cl–/OH–) exchanger activities in kidney proximal tubule.


1984 ◽  
Vol 35 (4) ◽  
pp. 397-401 ◽  
Author(s):  
Yoshihiko INAMORI ◽  
Yoshiaki KATO ◽  
Mayuri KUBO ◽  
Jun-ichi NAKANISHI ◽  
Mayumi NAKASHIMA ◽  
...  

1958 ◽  
Vol 195 (2) ◽  
pp. 343-346 ◽  
Author(s):  
E. J. Støren

Active uptake of PAH by rat renal cortex slices was studied by the method of Cross and Taggart. Uptake was determined at low and at high medium concentrations of PAH. Pentobarbital sodium in concentrations comparable to those found in plasma during anesthesia, significantly depressed the uptake of PAH on all occasions. Simultaneously oxygen consumption was reduced. Acetate failed to stimulate PAH uptake in the presence of pentobarbital, although tissue respiration was restored to normal.


1984 ◽  
Vol 67 (5) ◽  
pp. 529-534 ◽  
Author(s):  
P. K. Wirdnam ◽  
R. D. G. Milner

1. Rat kidney cortex slices were incubated for 30 min at 37°C in unmodified Krebs-Henseleit buffer containing aldosterone, vasopressin, theophylline, ethacrynic acid, frusemide, spironolactone or ouabain. 2. Tamm—Horsfall glycoprotein (THG) released into the media was measured by radioimmunoassay and at the end of each experiment the slices were homogenized and assayed for THG content. 3. Incubation of kidney cortex slices in unmodified buffer resulted in a significant increase in the slice THG content when compared with pre-incubation levels. The increase was prevented by puromycin or cycloheximide. 4. Incubation in ethacrynic acid (1 mmol/l) or frusemide (10 mmol/l) resulted in a significant increase in release of THG when compared with unmodified buffer. Puromycin or cycloheximide failed to prevent the increased release. 5. THG release induced by ethacrynic acid or frusemide is probably the result of an aggregation-disaggregation reaction on the cell membrane. It is suggested that the action of the chloride inhibiting diuretics, ethacrynic acid and frusemide, is mediated in some way via THG.


1978 ◽  
Vol 29 (2) ◽  
pp. 183-198 ◽  
Author(s):  
Myong Won Kahng ◽  
Irene K. Berezesky ◽  
Benjamin F. Trump

1964 ◽  
Vol 93 (1) ◽  
pp. 106-115 ◽  
Author(s):  
Samuel Thier ◽  
Maurice Fox ◽  
Leon Rosenberg ◽  
Stanton Segal

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