Effects of Certain Inhibitors on Renal Sodium Reabsorption and ATP Specific Activity

Kessler, Richard H.; Landwehr, DM; Quintanilla, A.; Weseley, Stephen A.; Kaufmann, W.; Arcila, Heriberto; Urbaitis, Barbara K.

doi:10.1159/000179657

Cited by 22 publications

(7 citation statements)

References 12 publications

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“…In a previous study [10] we reported that inorganic radiophosphate was incorporated into cortical ADP and A TP in a ratio of 3:4, a value consistent with adenylate kinase activity. This prediction is based on the incorporation of radiophosphate into ATP at the y position by phosphorylation of ADP.…”

Section: A D P^a M P + Atpsupporting

confidence: 64%

“…There are two possibilities: either most ATP in kidney tissue is used to energize sodium transport or there is an alter nate pathway that transforms chemical energy to transport work. Were the first possibility correct, it is difficult to explain the persistence of sodium reabsorption in the kidney that has been 'uncoupled' by the action of 2,4-dinitrophenol [8,10] or stressed by hypoxia [2] or by the administration of other materials that are actively transported.…”

Section: A D P^a M P + Atpmentioning

confidence: 99%

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Concentration of Adenine Nucleotide Compounds in Renal Cortex and Medulla

Urbaitis

Kessler²

1969

Nephron

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We describe a method of isolating and quantitating the nucleotide compounds of the renal cortex and inner medulla. Nucleotide concentrations were determined under conditions of saline administration, hydration and hydropenia. Adenosine phosphates were the dominant nucleotides and ATP equal in concentration in cortex and medulla in µmoles/g solids. AMP was abundant only in the cortex and was reciprocally related to the quantity of ATP. We cite this in evidence of adenylate kinase activity in the cortex. Concentrations of ATP/g solids were equal in both cortex and medulla in hydropenia and hydration. Calculations of energy for sodium transport based on these data are offered.

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Section: A D P^a M P + Atpsupporting

confidence: 64%

Section: A D P^a M P + Atpmentioning

confidence: 99%

Concentration of Adenine Nucleotide Compounds in Renal Cortex and Medulla

Urbaitis

Kessler²

1969

Nephron

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“…These factors would tend to elevate ATP concentrations and slow the rate of disappearance of ATP dur ing ischemia, causing an underestimation of the rate of ATP turnover [32]. During the first 2 min of ischemia, ATP concentrations fell from 1.45 pmol/g wet weight to 0.40 pmol/g wet weight; this is a change of 0.5 pmol/g/min and is similar to that described by Kessler [9].…”

Section: Discussionsupporting

confidence: 78%

Effects of Ischemia on Metabolite Concentrations in Dog Renal Cortex

Cunarro¹,

Schultz²,

Johnson³

et al. 1982

Kidney Blood Press Res

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To investigate the effects of ischemia on renal metabolites, sequential slices of renal cortex were removed during 5 min of renal artery occlusion and for 5 min after release of occlusion. ATP concentrations rapidly fell during ischemia and rose during the post-ischemic period. Based on the rate of decline of ATP concentrations, the rate of ATP production was estimated to be 0.5 µ mol ATP/g/min. This is considerably less than the rate of ATP production estimated from renal O₂ consumption. During ischemia, AMP concentrations rose, confirming the activity of adenylate kinase. The control lactate/pyruvate ratio suggested that dog kidney cytosol is more reduced than the cytosol of rat liver and kidney. During ischemia, the lactate concentrations and the lactate/pyruvate ratio of dog renal cortex increased as expected, and fell after restoration of blood flow. β-Hydroxybutyrate concentrations were considerably lower than those previously reported for rat liver and kidney. The β-hydroxybutyrate/acetoacetate ratio was not measurable during ischemia. However, the mitochondrial redox state, calculated from the glutamate/α-ketoglutarate·NH⁺₄ ratio, was similar to previous reports and this ratio appropriately changed during the ischemic and post-ischemic period.

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“…Most metabolic inhibitors which block ATP synthesis have been shown to affect sodium transport, for which about 80% of oxygen consumed by the kidney is utilized [58]. Cyanide, for example, when injected into the renal artery, decreases renal oxygen con sumption and sodium reabsorption [12,29,55,57] in a parallel fashion, but has no effect on Na-K-ATPase activity [1], Under these circumstances, cor tical ATP levels have been found to be depressed [29].…”

Section: Discussionmentioning

confidence: 99%

“…Since ATP is the specific substrate for this enzyme, generation of ATP might be a rate-limiting factor in active sodium transport. Thus, either inhibition of the enzyme [17,18,41] or inhibition of cellular energy production in the form of ATP [12,29,57] may result in decreased sodium reabsorption by the kidney.…”

Section: Introductionmentioning

confidence: 99%

Effect of Extracellular Volume Expansion on Renal Na-K-ATPase and Cell Metabolism

Kramer

Gonick²

1974

Nephron

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In the present study the reduction in renal fractional reabsorption of sodium from 99.6 ± 0.2 to 86.0 ± 3.3 % following ECV expansion with isotonic saline in the rat was associated with a small decrease in renal cortical Na-K-ATPase activity from 12.2 ± 0.5 to 10.8 ± 0.6 µmol Pi/mg protein/h and an increase in medullary enzyme activity from 23.3 ± 1.3 to 28.6 ± 1.8 µmol Pi/mg protein/h. In addition, an increase in cortical ATP concentration from 1.21 ± 0.12 to 1.55 ± 0.10 µmol/g wet weight was observed. These alterations resemble renal metabolic changes induced by low dose ouabain and favor the hypothesis that decreased tubular reabsorption of sodium following ECV expansion may be associated with alterations in active sodium transport.

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Effects of Certain Inhibitors on Renal Sodium Reabsorption and ATP Specific Activity

Cited by 22 publications

References 12 publications

Concentration of Adenine Nucleotide Compounds in Renal Cortex and Medulla

Concentration of Adenine Nucleotide Compounds in Renal Cortex and Medulla

Effects of Ischemia on Metabolite Concentrations in Dog Renal Cortex

Effect of Extracellular Volume Expansion on Renal Na-K-ATPase and Cell Metabolism

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