Stimulation of renal gluconeogenesis by inhibition of the sodium pump

Friedrichs, Dagmar; Schoner, Wilhelm

doi:10.1016/0304-4165(73)90123-2

Cited by 47 publications

(15 citation statements)

References 43 publications

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“…These observations were in accordance with the results of Friedrichs and Schoner [I 31 and similar to those obtained before with cyclic nucleotides [4]. Also in agreement with previous results obtained with Ado-3': 5'-P was the observation that norepinephrine was ineffective on glucose formation from glycerol (Table 1) and inhibitory on glucose formation from fructose [13]. These similarities in the actions of both substances could indicate that the stimulatory effect of norepinephrine might be mediated by Ado-3': 5'-P, in accordance with the previously described stimulatory effect of catecholamines on hepatic gluconeogenesis [18].…”

Section: The Stimulatory Effect Of Norepinephrine On Gluconeogenesis supporting

confidence: 83%

“…These results seem not to be in accordance with the above-mentioned hypothesis that Ado-3' : 5'-P was the intracellular messenger of norepinephrine, as recently suggested by Friedrichs and Schoner [13] a decrease of the stimulatory action on glucose formation from these particular substrates (see Fig. 1 and 2 and [4]).…”

Section: Comparison Ojthe Stimulatory Effect Of Norepinephrine With Tcontrasting

confidence: 49%

“…More recently Friedrichs and Schoner [13], Klahr et al [14], and Kurokawa and Massry [15] reported stimulatory effects of catecholamines on renal glucose formation in kidney cortex slices [14,15] or isolated kidney tubules [13], which these authors correlated with the stimulatory action of catecholamines on renal adenyl cyclase. This was substantiated by the finding that Ado-3': 5'-P levels of renal cortex as well as renal medulla were increased by isoproterenol and norepinephrine [5,9,15].…”

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confidence: 87%

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Metabolism of Isolated Kidney Tubules Independent Actions of Catecholamines on Renal Cyclic Adenosine 3′: 5′‐Monophosphate Levels and Gluconeogenesis

Guder

Rupprecht

1975

European Journal of Biochemistry

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Isolated kidney cortex tubules from starved rats have been used to study the actions of catecholamines on renal adenosine 3' : 5'-monophosphate (Ado-3' : 5'-P) levels and gluconeogenesis.In accordance with previous workers, norepinephrine was found to increase glucose formation from lactate and pyruvate and to a smaller degree from malate, succinate, fumarate, glutamate and glutamine. The stimulatory effect of 0.5 pM norepinephrine was additive to that of 0.1 mM Ado-3' : 5'-P, indicating an Ado-3' : 5'-P-independent mechanism of catecholamine action. The effects of parathyroid hormone and oleate on gluconeogenesis were also additive to that of norepinephrine.A comparative study of the actions of different catecholamine derivatives revealed that gluconeogenesis was stimulated in parallel to the a-adrenergic potency of the hormones, whereas Ado-3' : 5'-P levels were increased according to the known P-stimulatory potency of the agents. Although isoproterenol was by far the most effective in raising Ado-3': 5'-P levels, it was without effect on glucose formation from pyruvate, when added at 0.1 pM. At the same concentration, phenylephrine, which had no effect on Ado-3': 5'-P levels, was the best stimulator of gluconeogenesis.The a-receptor blocking agent phentolamine inhibited the stimulatory effect of catecholamines on gluconeogenesis with a 50 times higher potency than propranolol, a P-blocking agent. The fact that the stimulatory effect of Ado-3': 5'-P was also blocked by propranolol, indicated an unspecific mechanism of action of this substance. The results indicate that the stimulatory effect of catecholamines on renal gluconeogenesis are mediated by an a-receptor and that they are independent from the stimulation of renal adenyl cyclase by these agents.

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Section: The Stimulatory Effect Of Norepinephrine On Gluconeogenesis supporting

confidence: 83%

Section: Comparison Ojthe Stimulatory Effect Of Norepinephrine With Tcontrasting

confidence: 49%

mentioning

confidence: 87%

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Metabolism of Isolated Kidney Tubules Independent Actions of Catecholamines on Renal Cyclic Adenosine 3′: 5′‐Monophosphate Levels and Gluconeogenesis

Guder

Rupprecht

1975

European Journal of Biochemistry

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“…Indeed, inhibition of Na þ -K þ -ATPase and, hence, a decrease in sodium tubule transport by the kidney is associated with increased rates of gluconeogenesis [9]. These findings suggest that energy-requiring processes, such as renal growth, sodium transport and gluconeogenesis compete for the available energy in nephron tubules and could explain the striking natriuresis observed under chronic acidosis [1].…”

Section: Introductionmentioning

confidence: 67%

Effects of NH4Cl-induced systemic metabolic acidosis on kidney mitochondrial coupling and calcium transport in rats

Bento

Fagian

Vercesi

et al. 2007

Nephrology Dialysis Transplantation

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Background. We have previously shown that chronic metabolic acidosis, induced in rats by NH 4 Cl feeding, leads to nephron hypertrophy and to a decreased water-salt reabsorption by the kidneys. Since mitochondria are the main source of metabolic energy that drives ion transport in kidney tubules, we examined energy-linked functions (respiration, electrochemical membrane potential and coupling between respiration and ADP phosphorylation) in mitochondria isolated from rat kidney and liver at 48 h after metabolic acidosis induced by NH 4 Cl. Methods. Mitochondria isolated from the kidneys and liver of metabolic acidotic rats, induced by NH 4 Cl, was used to study of the oxygen consumption by Clarktype electrode, mitochondrial electrical transmembrane potential estimated by the safranine O method and the variations in free medium Ca 2+ concentrations examined by absorbance spectrum of Arsenazo III set at the 675-685 nm wavelength pair. Results. Whole kidney and liver mitochondria isolated from 48 h acidotic rats presented higher resting respiration, lower respiratory control and a lower ADP/O ratio than controls. These differences in mitochondrial coupling, between respiration and oxidative phosphorylation (ATP synthesis), were totally corrected when experiments were carried out in the presence of carboxyatractyloside, GDP and BSA, indicating that mitochondrial uncoupling proteins are more active in acidotic rat kidneys. Interestingly, determination of Ca 2þ transport demonstrated a faster rate of initial Ca 2þ uptake by acidotic kidney mitochondria, which resulted in a lower concentration of extra-mitochondrial Ca 2þ under steady-state conditions (Ca 2þ set point) when compared with control mitochondria.In contrast, there were no significant differences in the rates of Na þ or ruthenium red induced Ca 2þ efflux. Conclusions. We suggest that the mild uncoupling and higher Ca 2þ accumulation represents an adaptation of the mitochondria to cope with conditions of oxidative stress and high cytosolic Ca 2þ , which are associated with a decreased efficiency of oxidative phosphorylation that may explain, at least in part, the striking natriuresis observed under chronic acidosis. Finally, there were no changes in Ca 2þ transport or coupling in liver mitochondria isolated from the acidotic rats.

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“…Studies using isolated proximal tubules have shown that enhanced glutamine metabolism and ammonia production are linked to increased gluconeogenesis (22). On the other hand, maneuvers that inhibit Na + -K + -ATPase, and hence sodium tubule transport by the kidney, stimulate gluconeogenesis (23,24). Since metabolic acidosis results in a lower filtered load of bicarbonate and consequently in less bicarbonate being reabsorbed, and since decreased Na + -H + antiporter activity is associated with stimulated gluconeogenesis, the overall effect should be dissipation of the Na + electrochemical gradient leading to a decreased reabsorption of Na + as observed in the present study.…”

Section: Groupsmentioning

confidence: 99%

Effect of metabolic acidosis on renal tubular sodium handling in rats as determined by lithium clearance

Menegon

Figueiredo

Gontijo³

1998

Braz J Med Biol Res

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Systemic metabolic acidosis is known to cause a decrease in salt and water reabsorption by the kidney. We have used renal lithium clearance to investigate the effect of chronic, NH 4 Cl-induced metabolic acidosis on the renal handling of Na + in male Wistar-Hannover rats (200-250 g). Chronic acidosis (pH 7.16 ± 0.13) caused a sustained increase in renal fractional Na + excretion (267.9 ± 36.4%), accompanied by an increase in fractional proximal (113.3 ± 3.6%) and postproximal (179.7 ± 20.2%) Na + and urinary K + (163.4 ± 5.6%) excretion when compared to control and pair-fed rats. These differences occurred in spite of an unchanged creatinine clearance and Na + filtered load. A lower final body weight was observed in the acidotic (232 ± 4.6 g) and pair-fed (225 ± 3.6 g) rats compared to the controls (258 ± 3.7 g). In contrast, there was a significant increase in the kidney weights of acidotic rats (1.73 ± 0.05 g) compared to the other experimental groups (control, 1.46 ± 0.05 g; pair-fed, 1.4 ± 0.05 g). We suggest that altered renal Na + and K + handling in acidotic rats may result from a reciprocal relationship between the level of metabolism in renal tubules and ion transport.

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Stimulation of renal gluconeogenesis by inhibition of the sodium pump

Cited by 47 publications

References 43 publications

Metabolism of Isolated Kidney Tubules Independent Actions of Catecholamines on Renal Cyclic Adenosine 3′: 5′‐Monophosphate Levels and Gluconeogenesis

Metabolism of Isolated Kidney Tubules Independent Actions of Catecholamines on Renal Cyclic Adenosine 3′: 5′‐Monophosphate Levels and Gluconeogenesis

Effects of NH4Cl-induced systemic metabolic acidosis on kidney mitochondrial coupling and calcium transport in rats

Effect of metabolic acidosis on renal tubular sodium handling in rats as determined by lithium clearance

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