scholarly journals 3-Mercaptopicolinic acid, an inhibitor of gluconeogenesis

1974 ◽  
Vol 138 (3) ◽  
pp. 387-394 ◽  
Author(s):  
N. W. DiTullio ◽  
C. E. Berkoff ◽  
B. Blank ◽  
V. Kostos ◽  
E. J. Stack ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Diabetic Rats ◽  
Kidney Cortex ◽  
Hepatic Glycogen ◽  
Hypoglycaemic Effect ◽  
Rat Kidney Cortex ◽  
Urea Production ◽  
Rat Livers

1. 3-Mercaptopicolinic acid (SK&F 34288) inhibited gluconeogenesis in vitro, with lactate as substrate, in rat kidney-cortex and liver slices. 2. In perfused rat livers, gluconeogenesis was inhibited when lactate, pyruvate or alanine served as substrate, but not with fructose, suggesting pyruvate carboxylase or phosphoenolpyruvate carboxylase as the site of inhibition. No significant effects were evident in O2 consumption, hepatic glycogen, urea production, or [lactate]/[pyruvate] ratios. 3. A hypoglycaemic effect was evident in vivo in starved and alloxan-diabetic rats, starved guinea pigs and starved mice, but not in 4h-post-absorptive rats. 4. In the starved rat the hypoglycaemia was accompanied by an increase in blood lactate. 5. A trace dose of [14C]lactate in vivo was initially oxidized to a lesser extent in inhibitor-treated rats, but during 90min the total CO2 evolved was slightly greater. The total amount of the tracer oxidized was not significantly different from that in the controls.

scholarly journals Accumulation of Sulfate by Mitochondria of Rat Kidney Cortex

1962 ◽  
Vol 45 (4) ◽  
pp. 757-775 ◽  
Author(s):  
Robert W. Winters ◽  
Adelaide M. Delluva ◽  
Ingrith J. Deyrup ◽  
Robert E. Davies
Keyword(s):  
Rat Kidney ◽  
Kidney Cortex ◽  
Ph Optimum ◽  
Rat Kidney Cortex ◽  
Sulfate Ions ◽  
Straight Line ◽  
Freundlich Adsorption Isotherm ◽  
Ambient Concentrations

Twice washed mitochondria from rat kidney cortex can accumulate sulfate ions from low (10-7 M) ambient concentrations to create virtual gradients of several hundred to one. This sulfate is subsequently released. The activation energy for the uptake is 12,000 calories per mole; for release it is about 30,000 calories per mole. Variations in the sulfate concentration of the medium show that there is a straight line Freundlich adsorption isotherm over a million-fold range of concentration of sulfate in the medium. There are 9 x 104 sites at 10-5 M and 9 x 105 sites at 10-3 M sulfate per average single mitochondrion. Preincubation at 30°C rapidly destroys the ability to accumulate sulfate. Partial protection occurs if oxidative phosphorylation is proceeding during the preincubation. The concentration of the endogenous inorganic sulfate of twice washed mitochondria is 4.2 x 10-4 moles per liter of mitochondrial pellet water; 99.85 per cent of this endogenous sulfate is inexchangeable with external sulfate in vitro. It is all exchangeable in vivo. The pH optimum for accumulation of radiosulfate from dilute external sulfate concentrations is 5.5. These observations show that there is a delicate and specific mechanism in mitochondria from kidney cortex which accumulates sulfate. The chemical nature of the accumulated sulfate is unknown.

Effect on kidney S35O4 uptake of compounds related to SO4 transport and metabolism

1964 ◽  
Vol 207 (1) ◽  
pp. 84-88 ◽  
Author(s):  
Ingrith J. Deyrup
Keyword(s):  
Amino Acids ◽  
Rat Kidney ◽  
Point Of View ◽  
Transport Systems ◽  
Kidney Cortex ◽  
Cellular Transport ◽  
Rat Kidney Cortex ◽  
Aryl Sulfatase

Experiments have been carried out to test the effects on S35O4 accumulation by rat kidney cortex slices in vitro of 1) compounds known to affect renal SO4 reabsorption (thiosulfate, amino acids); 2) compounds secreted by the kidney, or known to affect specific cellular transport systems (including tetraethylammonium ions, guanidine, creatinine, carinamide, probenecid, phloretin, diethylstilbestrol, ethylenediaminetetraacetate sodium); and 3) compounds related to SO4 metabolism (aryl sulfatase substrates). Under the conditions of the experiment, net S35O4 uptake was depressed by thiosulfate, certain amino acids, carinamide, phloretin, diethylstilbestrol, and aryl sulfatase substrates. It was enhanced by ethylenediaminetetraacetate sodium. Other compounds were without effect. These results are discussed from the point of view of the possible relationship between SO4 accumulation in vitro and transport in vivo.

scholarly journals FURTHER OBSERVATIONS ON UPTAKE OF S35-LABELLED SULFATE BY RENAL TISSUE IN VITRO

1956 ◽  
Vol 39 (6) ◽  
pp. 893-908 ◽  
Author(s):  
Ingrith J. Deyrup
Keyword(s):  
Rat Kidney ◽  
Mammalian Species ◽  
Renal Tissue ◽  
Metabolic Inhibitors ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Lower Vertebrates ◽  
The One

Additional studies have been made of the accumulation of S35 by renal cortical tissue incubated in media containing radiosulfate. This process was found to occur in several mammalian species in addition to the rat, but was not observed as a significant occurrence in three species of lower vertebrates. In the case of rat renal tissue, S35 uptake was found to be sensitive to the pH and osmolar concentration of the medium. The character of the anions present in conjunction with K+ affected it as well. Various factors known to be related to in vitro accumulative processes, as well as to renal sulfate reabsorption by the intact dog, were tested on rat kidney cortex to assess the effect on radiosulfate uptake. In general, all substances tested (amino acids, metabolic intermediates, ATP, metabolic inhibitors, competitive inhibitors for PAH accumulation in vitro) were found to lessen S35 uptake, or to be without effect upon it. The one striking exception was phlorhizin, which enhanced markedly S35 uptake in vitro, as it does sulfate reabsorption in vivo. Some implications of these findings have been discussed.

Identification of an apical \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{Cl}^{-}{/}\mathrm{HCO}_{3}^{-}\) \end{document} exchanger in rat kidney proximal tubule

2003 ◽  
Vol 285 (3) ◽  
pp. C608-C617 ◽  
Author(s):  
Snezana Petrovic ◽  
Liyun Ma ◽  
Zhaohui Wang ◽  
Manoocher Soleimani
Keyword(s):  
Proximal Tubule ◽  
Apical Membrane ◽  
Rat Kidney ◽  
Proximal Tubules ◽  
Immunocytochemical Staining ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Kidney Proximal Tubule ◽  
Anion Transporter

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.

scholarly journals The Effect of Racemomycin-D, a Nephrotoxic Antibiotic, on Cellular Metabolism of Rat Kidney Cortex in Vitro

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

Effect of Pentobarbital Sodium on Uptake of PAH by Rat Kidney Cortex Slices in Vitro

1958 ◽  
Vol 195 (2) ◽  
pp. 343-346 ◽  
Author(s):  
E. J. Støren
Keyword(s):  
Oxygen Consumption ◽  
Renal Cortex ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Tissue Respiration ◽  
Rat Kidney Cortex ◽  
Pentobarbital Sodium ◽  
Cortex Slices ◽  
Kidney Cortex Slices

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.

Regulation of sgk by aldosterone and its effects on the epithelial Na+ channel

2000 ◽  
Vol 278 (4) ◽  
pp. F613-F619 ◽  
Author(s):  
Alexander Shigaev ◽  
Carol Asher ◽  
Hedva Latter ◽  
Haim Garty ◽  
Eitan Reuveny
Keyword(s):  
De Novo ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Na Channel ◽  
Xenopus Laevis Oocytes ◽  
Fourfold Increase ◽  
Tight Epithelia ◽  
High Level

Aldosterone is the major corticosteroid regulating Na+ absorption in tight epithelia and acts primarily by activating the epithelial Na+ channel (ENaC) through unknown induced proteins. Recently, it has been reported that aldosterone induces the serum- and glucocorticoid-dependent kinase sgk and that coexpressing ENaC with this kinase in Xenopus laevis oocytes increases the amiloride-sensitive Na+current (Chen SY, Bhargava A, Mastroberardino L, Meijer OC, Wang J, Buse P, Firestone GL, Verrey F, and Pearce D. Proc Natl Acad Sci USA 96: 2514–2519, 1999). The present study was done to further characterize regulation of sgk by aldosterone in native mammalian epithelia and to examine its effect on ENaC. With both in vivo and in vitro protocols, an almost fivefold increase in the abundance of sgk mRNA has been demonstrated in rat kidney and colon but not in lung. Induction of sgk by aldosterone was detected in kidney cortex and medulla, whereas the papilla expressed a constitutively high level of the kinase. The increase in sgkmRNA was detected as early as 30 min after the hormonal application and was independent of de novo protein synthesis. The observed aldosterone dose-response relationships suggest that the response is mediated, at least in part, by occupancy of the mineralocorticoid receptor. Coexpressing sgk and ENaC in Xenopus oocytes evoked a fourfold increase in the amiloride-blockable Na+ channel activity. A point mutation in the β-subunit known to impair regulation of the channel by Nedd4 (Y618A) had no significant effect on the response to sgk.

Tamm—Horsfall Glycoprotein Release from Rat Kidney Cortex Slices in Vitro

1984 ◽  
Vol 67 (5) ◽  
pp. 529-534 ◽  
Author(s):  
P. K. Wirdnam ◽  
R. D. G. Milner
Keyword(s):  
Cell Membrane ◽  
Ethacrynic Acid ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
The Media ◽  
Cortex Slices ◽  
Kidney Cortex Slices ◽  
Krebs Henseleit Buffer

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.

Metabolic and ultrastructural response of rat kidney cortex to in vitro ischemia

1978 ◽  
Vol 29 (2) ◽  
pp. 183-198 ◽  
Author(s):  
Myong Won Kahng ◽  
Irene K. Berezesky ◽  
Benjamin F. Trump
Keyword(s):  
Rat Kidney ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
In Vitro Ischemia
Sign in / Sign up

Export Citation Format

Share Document