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.

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.

RENIN SECRETION IN VITRO FROM RAT KIDNEY CORTEX SLICES

1969 ◽  
Vol 60 (3) ◽  
pp. 550-554 ◽  
Author(s):  
Lj. Božović ◽  
S. Efendić
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Active Mechanism ◽  
Cortex Slices ◽  
Kidney Cortex Slices

ABSTRACT A method for in vitro studies of renin release is described. Kidney cortex slices taken from control rats and rats stimulated to release renin were incubated with and without glucose. Renin release from the slices to a large extent was glucose-dependent. This result supports the hypothesis of an active mechanism of renin secretion.

Effect of metal ions on in vitro gluconeogenesis in rat kidney cortex slices

1965 ◽  
Vol 208 (5) ◽  
pp. 841-846 ◽  
Author(s):  
Julia Z. Rutman ◽  
Lawrence E. Meltzer ◽  
J. Roderick Kitchell ◽  
Robert J. Rutman ◽  
Philip George
Keyword(s):  
Amino Acids ◽  
Metal Ions ◽  
Tricarboxylic Acid Cycle ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
In Vitro Systems ◽  
Cortex Slices ◽  
Kidney Cortex Slices

The effect of metal ions on glucose formation from amino acids and glycolytic and tricarboxylic acid cycle intermediates has been examined in rat kidney cortex slices in vitro. Of the metals tested, only Mn++ and Ca++ have been shown to be stimulatory, while Zn++, Cu++, and Cd++ are inhibitory. The case of Mn++ activation is of particular interest because Mg++ ions are inactive in this system, despite the similarities usually observed in the in vitro systems. The stimulation of gluconeogenesis from α-keto acids is comparable for both Ca++ and Mn++, in contrast to the lack of a Mn++ effect with the homologous l-α-amino acids. Evidence is presented as to the possible significance of metal ions in regulating carbohydrate metabolism.

scholarly journals The interrelationship of the concentration of hydrogen ions, bicarbonate ions, carbon dioxide and calcium ions in the regulation of renal gluconeogenesis in the rat

1973 ◽  
Vol 136 (3) ◽  
pp. 445-453 ◽  
Author(s):  
George A. O. Alleyne ◽  
Hernando Flores ◽  
Anne Roobol
Keyword(s):  
Phosphoenolpyruvate Carboxylase ◽  
Rat Kidney ◽  
Respiratory Acidosis ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Bicarbonate Ions ◽  
Cortex Slices ◽  
Glucose Formation ◽  
Kidney Cortex Slices

1. The interrelationship of acidosis and Ca2+on the stimulation of gluconeogenesis by rat kidney-cortex slices was studied. 2. Ca2+stimulated gluconeogenesis from glutamine, glutamate, 2-oxoglutarate, succinate, malate, pyruvate, lactate and fructose, but not from galactose. 3. The [Ca2+] needed for optimum gluconeogenesis was about 2mm, but at this concentration, acidosis, produced in vitro by a decrease of [HCO3−] in the medium at constant pCO2 or by an increase in pCO2 at constant [HCO3−], did not stimulate gluconeogenesis. 4. In the absence of Ca2+, acidosis (low [HCO3−]) stimulated gluconeogenesis from glutamine, glutamate, 2-oxoglutarate, succinate, malate, pyruvate and lactate but not from fructose or galactose. With succinate as substrate, the stimulatory effect of acidosis (low [HCO3−]) disappeared at Ca2+concentrations above 1.0mm. 5. The [HCO3−] was the most important determinant of the acidosis effect since a decrease of pH caused by an increase in pCO2 did not uniformly stimulate gluconeogenesis, whereas a decrease in [HCO3−] without a change in pH consistently stimulated glucose formation in a way similar to the stimulation produced by acidosis (low [HCO3−]) in the absence of Ca2+. 6. Acidosis in vitro inhibited the rate of decrease of activity of phosphoenolpyruvate carboxylase in slices, and Ca2+caused an increase in the activity of fructose 1-phosphate aldolase. 7. Respiratory acidosis in vitro caused an increase in the activity of phosphoenolpyruvate carboxylase in kidney cortex and an increase in gluconeogenesis from glutamine. 8. Possible points of interaction between Ca2+, H+and HCO3−with the gluconeogenic sequence are discussed.

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