Effect of bicarbonate on glutamine and glutamate metabolism by rat kidney cortex mitochondria

1985 ◽  
Vol 249 (4) ◽  
pp. F573-F581
Author(s):  
R. C. Scaduto ◽  
A. C. Schoolwerth
Keyword(s):  
Rat Kidney ◽  
Competitive Inhibitor ◽  
Kidney Cortex ◽  
Mitochondrial Enzymes ◽  
Glutamate Metabolism ◽  
Bicarbonate Buffer ◽  
Rat Kidney Cortex ◽  
Glutamate Oxalacetate Transaminase ◽  
Stimulation Of

Isolated rat kidney cortex mitochondria were incubated at pH 7.4 in the presence or absence of a CO2/bicarbonate buffer (28 mM) to investigate the pH-independent role of bicarbonate on glutamine and glutamate metabolism. Changes in the concentration of key intermediates and products during the incubations were used to calculate metabolite flux rates through specific mitochondrial enzymes. With 1 mM glutamine and 2 mM glutamate as substrates, bicarbonate caused an inhibition of glutamate oxalacetate transaminase flux and a stimulation of glutamate deamination. The same effects were also produced with addition of either aminooxyacetate or malonate. These effects of bicarbonate were prevented when 0.2 mM malate was included as an additional substrate. Bicarbonate ion was identified as a potent competitive inhibitor of rat kidney cortex succinate dehydrogenase. These results indicate that aminooxyacetate, malonate, and bicarbonate all act to stimulate glutamate deamination through a suppression of glutamate transamination, and that the control by transamination of glutamate deamination is due to alterations in alpha-ketoglutarate metabolism. In contrast, in mitochondria incubated with glutamine in the absence of glutamate, bicarbonate was found to inhibit glutamate dehydrogenase flux. This effect was found to be due in part to the lower intramitochondrial pH observed in incubations with bicarbonate. These findings indicate that bicarbonate ion, independent of pH, may have an important regulatory role in renal glutamine and glutamate metabolism.

scholarly journals Na+-gradient-dependent stimulation of renal transport of ρ-aminohippurate

1982 ◽  
Vol 208 (1) ◽  
pp. 243-246 ◽  
Author(s):  
M I Sheikh ◽  
J V Møller
Keyword(s):  
Rat Kidney ◽  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Cortex Slices ◽  
Kidney Cortex Slices ◽  
Stimulation Of

Transport of rho-aminohippurate was studied by the use of a preparation of rabbit kidney basolateral-membrane vesicles and in rat kidney-cortex slices under anaerobic conditions. With both preparations clear evidence of Na+-gradient stimulation of rho-aminohippurate transport (‘overshoot’) was obtained. These results thus indicate that a significant aspect of active rho-aminohippurate transport is by co-transport with Na+, and they appear to resolve previous disagreements concerning the role of Na+. Vesicle studies with a potential-sensitive dye suggested that rho-aminohippurate may be transported electroneutrally, i.e. in a 1:1 complex with Na+.

scholarly journals Transcriptional regulation by glucocorticoids of mitochondrial oxidative enzyme genes in the developing rat kidney

1996 ◽  
Vol 315 (2) ◽  
pp. 555-562 ◽  
Author(s):  
Fatima DJOUADI ◽  
Jean BASTIN ◽  
Daniel P. KELLY ◽  
Claudie MERLET-BENICHOU
Keyword(s):  
Fatty Acid ◽  
Molecular Mechanisms ◽  
Tricarboxylic Acid Cycle ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Transcriptional Level ◽  
Mitochondrial Enzymes ◽  
Mrna Levels ◽  
Rat Kidney Cortex ◽  
Mitochondrial Fatty Acid

Mitochondrial fatty acid β-oxidation plays a major role in providing the ATP required for reabsorptive processes in the adult rat kidney. However, the molecular mechanisms and signals involved in induction of the enzymes of fatty acid oxidation during development in this and other organs are unknown. We therefore studied the changes in the steady-state levels of mRNA encoding medium-chain acyl-CoA dehydrogenase (MCAD), which catalyses the initial step in mitochondrial fatty acid β-oxidation, in the rat kidney cortex and medulla between postnatal days 10 and 30. Furthermore, we investigated whether the expression of MCAD and of mitochondrial malate dehydrogenase (mMDH), a key enzyme in the tricarboxylic acid cycle, might be co-ordinately regulated by circulating glucocorticoids in the immature kidney during development. In the cortex, the levels of MCAD mRNA rose 4-fold between day 10 and day 21, and then decreased from day 21 to day 30. In the medulla a postnatal increase in the concentration of MCAD mRNA (8-fold) was observed during the same period. Adrenalectomy prevented the 16–21-day developmental increases in MCAD and mMDH mRNA levels in the cortex and medulla; these could be restored by dexamethasone treatment. A single injection of dexamethasone into 10-day-old rats led to a rise in MCAD and mMDH mRNA levels in the renal cortex due to stimulation of gene transcription, as shown by nuclear run-on assays. Therefore MCAD and mMDH gene expression is tightly regulated at the transcriptional level by developmental changes in circulating glucocorticoid levels. These hormones might thus represent a good candidate as a co-ordinating factor in the expression of nuclear genes encoding mitochondrial enzymes in the kidney during postnatal development.

scholarly journals Inositol lipid signalling occurs in brush-border membranes during initiation of compensatory renal growth in the rat

1993 ◽  
Vol 295 (2) ◽  
pp. 599-605 ◽  
Author(s):  
H Banfić ◽  
M Vuica ◽  
M Knotek ◽  
S Moslavac ◽  
N Divecha
Keyword(s):  
Brush Border ◽  
Plasma Membranes ◽  
Rat Kidney ◽  
Unilateral Nephrectomy ◽  
Kidney Cortex ◽  
Compensatory Renal Growth ◽  
Rat Kidney Cortex ◽  
Contralateral Kidney ◽  
Inositol Lipids ◽  
Stimulation Of

Using highly specific mass assays, concentrations of inositol lipids and 1,2-diacylglycerol (DAG) were determined in plasma membranes isolated from rat kidney cortex. Significantly higher concentrations of inositol lipids were determined in brush-border (BBM) than in basal-lateral (BLM) plasma membranes, although DAG concentrations were similar in both. After unilateral nephrectomy, a decrease in PtdIns(4,5)P2 and PtdIns4P, with a concomitant increase in DAG and translocation of protein kinase C (PKC), were observed in BBM but not in BLM isolated from the remaining kidney. On the other hand, stimulation of renal cortical slices with insulin-like growth factor II (IGF-II) or phenylephrine caused similar effects in BLM but not in BBM. Stimulation of phospholipase C activity with translocation of PKC only to BBM in one kidney was also induced by occlusion of blood flow through the contralateral kidney for 15 min. At 30 min after the occlusion was removed and reflow established, DAG concentration and the amount of PKC in BBM returned to control values. These results suggest that an early signal after unilateral nephrectomy is transmitted to cells through BBM and can be switched on and off by blood occlusion and reflow through the contralateral kidney, while hormonal signals caused by IGF-II and phenylephrine are transmitted to cells through BLM.

Inhibitory Role of Ca2+ in the Control of Renin Secretion: A Study Using Supervised Dispersed Rat Renal Cortical Cells

1989 ◽  
Vol 77 (3) ◽  
pp. 273-279 ◽  
Author(s):  
Karen Pardy ◽  
B. C. Williams ◽  
A. R. Noble
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Kidney Cortex ◽  
Cortical Cells ◽  
Rat Kidney Cortex ◽  
Cyclic Monophosphate ◽  
Cortex Cell ◽  
The Mean

1. The role of Ca2+ in the control of renin release was investigated using a collagenase-dispersed rat kidney cortex cell preparation. 2. Superfusion with a series of low [Ca2+] buffers in either ascending or descending order of concentration increased renin release. Exposure to 0.06 mmol/l Ca2+ increased release by 120% (P < 0.001) when presented as the first buffer in ascending order of concentration and by 79% (P < 0.001) when presented as the fourth and last in a series of descending order. 3. The Ca2+ entry blocking drug diltiazem in a range of concentrations increased renin release and at 10−5 mol/l diltiazem the mean stimulation was 35% (P < 0.01). 4. 8-(N,N-Diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) reduces the release of Ca2+ from intracellular stores and, studied over a range of concentrations, this compound increased renin release. At 10−5 mol/l TMB-8 the mean increase was 44% (P < 0.001). 5. None of these experimental manipulations, low [Ca2+], diltiazem or TMB-8, had any effect on the release of adenosine 3′:5′-cyclic monophosphate into the cell superfusate, indicating that a decrease in intracellular [Ca2+] increases renin release by a mechanism which is independent of changes in adenosine 3′:5′-cyclic monophosphate production. 6. Effects of low [Ca2+], diltiazem and TMB-8 on renin secretion were all shown to be reversible when superfusion with control buffer was resumed.

Stimulation of ouabain-sensitive86Rb+uptake and Na+,K+-ATPase α-subunit phosphorylation by a cAMP-dependent signalling pathway in intact cells from rat kidney cortex

FEBS Letters ◽  
1996 ◽  
Vol 396 (2-3) ◽  
pp. 309-314 ◽  
Author(s):  
Maria Luisa Carranza ◽  
Eric Féraille ◽  
Militza Kiroytcheva ◽  
Martine Rousselot ◽  
Hervé Favre
Keyword(s):  
Rat Kidney ◽  
Signalling Pathway ◽  
Kidney Cortex ◽  
Intact Cells ◽  
Α Subunit ◽  
Rat Kidney Cortex ◽  
Stimulation Of

DDT-Induced Stimulation of Key Gluconeogenic Enzymes In Rat Kidney Cortex

1972 ◽  
Vol 50 (2) ◽  
pp. 225-229 ◽  
Author(s):  
S. Kacew ◽  
R. L. Singhal ◽  
G. M. Ling
Keyword(s):  
Pyruvate Carboxylase ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Glucocorticoid Hormones ◽  
Rat Kidney Cortex ◽  
Gluconeogenic Enzymes ◽  
Maximal Stimulation ◽  
Adrenalectomized Rats ◽  
Stimulation Of

Administration of technical DDT or o,p′-DDT produced marked increases in pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose-1,6-diphosphatase, and glueose-6-phospfaatase activities in rat kidney cortex. Significant increases in these key gluconeogenic enzymes occurred at 2–3 days and maximal stimulation was seen 5–7 days after the beginning of o,p′-DDT treatment. This DDT isomer, when given to adrenalectomized rats, produced increases in renal enzymes similar to those observed in intact animals. Furthermore, since administration of triamcinolone to o,p′-DDT-treated rats failed to potentiate the action of this insecticide on various enzymes, evidence indicates that the stimulation of kidney cortex gluconeogenesis by DDT is not mediated through a release of glucocorticoid hormones from the adrenal cortex.

scholarly journals PPARα Gene Expression in the Developing Rat Kidney: Role of Glucocorticoids

2001 ◽  
Vol 12 (6) ◽  
pp. 1197-1203
Author(s):  
FATIMA DJOUADI ◽  
JEAN BASTIN
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Culture Media ◽  
Rat Kidney ◽  
Fold Increase ◽  
Kidney Cortex ◽  
Peroxisome Proliferator ◽  
Rat Kidney Cortex

Abstract. The α isoform of peroxisome proliferator-activated receptor (PPARα), which is highly expressed in the kidney, can stimulate the expression of genes that are involved in fatty acid catabolism and therefore might be involved in the control of renal fatty acid β-oxidation. PPARα expression and its regulation in the immature kidney are not well documented. This study delineated the developmental pattern of PPARα expression in the rat kidney cortex and the medulla between postnatal days 10 and 30 and investigated the role of glucocorticoids in regulating PPARα expression. In the cortex, PPARα mRNA and protein increased 2- and 1.8-fold, respectively, from 10 to 21 d and then decreased 1.5- and 2.4-fold from 21 to 30 d. In the medulla, PPARα mRNA and protein increased continuously 3.3- and 2.4-fold, respectively. It is shown here that acute treatment by dexamethasone of 10-d-old rats precociously induced a 4- to 6-fold increase in PPARα mRNA and a 1.8-fold increase in protein within 6 h in each part of the kidney. Chronic injection of dexamethasone for 3 d also increased PPARα mRNA 3.8- and 2.2-fold in the cortex and the medulla, respectively, with a 1.5- and 2-fold increase in protein. Furthermore, adrenalectomy prevented the increases in PPARα mRNA and protein in both the cortex and the medulla between postnatal days 16 and 21, and these could be restored by dexamethasone treatment. Finally, with the use of an established renal cell line, it was shown that glucocorticoids stimulate gene expression of PPARα and of medium chain acyl-CoA dehydrogenase (MCAD, a PPARα target gene) 2- to 4-fold and 1.5-fold, respectively, and that addition of fatty acids in the culture media led to a 2.2-fold increase in MCAD mRNA. Altogether, these results demonstrated that glucocorticoids are potent regulators of PPARα development in the immature kidney and that these hormones act in concert with fatty acids to regulate MCAD gene expression in renal cells.

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