Effects of Chlormerodrin, p-Chloromercuribenzoate and Dichlorphenamide on Renal Sodium Reabsorption and Oxygen Consumption

Kessler, Richard H.; Weinstein, S. W.; Nash, Franklin D.; Fujimoto, M

doi:10.1159/000179335

Cited by 14 publications

(3 citation statements)

References 8 publications

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“…Unlike cyanide (12), chlorothiazi de (23) or organic mercurial diuretic compounds (16), it has no effect on renal oxygen consumption and, in the present study, did not alter the 32P 0 4 uptake by the adenine nucleotides.…”

Section: Discussioncontrasting

confidence: 50%

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

Kessler¹,

Landwehr²,

Quintanilla³

et al. 1968

Nephron

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Sodium reabsorption in the kidney should be as closely related to ATP synthesis as it is to oxygen consumption. This problem was investigated in the present studies with the assumption that the uptake of inorganic phosphate by ATP is related to the rate of ATP synthesis. Radiophosphate was infused into anesthetized dogs in the course of renal clearance studies. The experimental protocols included the administration of compounds known to affect sodium reabsorption or renal cortical metabolism. At the termination of the function study, the renal cortices were removed and their nucleotides separated by column chromatography. The specific activity of ATP and sodium reabsorption in control studies were compared to values obtained in experimental studies. Sodium reabsorption was reduced with and without an effect on the specific activity of ATP. Conversely, ATP specific activity was reduced with and without an effect on sodium reabsorption. We conclude that a part of cortical sodium reabsorption can be energized other than by ATP metabolism.

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Section: Discussioncontrasting

confidence: 50%

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

Kessler¹,

Landwehr²,

Quintanilla³

et al. 1968

Nephron

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“…Some studies of the effects of maneuvers that reduced T Na ϩ [e.g., reduced arterial pressure and/or renal blood flow (RBF) or the administration of diuretics] were excluded because of the unavailability of information on GFR and/or TNaϩ (10,11,18,20,26,32,36,37,59,75,78). Others were excluded because GFR was not reduced to zero and T Na ϩ was not measured or because there was no analysis of the relationship between GFR or T Na ϩ and V O 2 total from which basal percent renal V O2 could be derived (1,21,22,25,28,46,50,53,56,63,64,67,76,77) or because no significant correlation was observed between T Na ϩ and V O 2 total (47). We also excluded studies in which both renal V O 2 total and TNaϩ were measured, but the latter were not varied sufficiently to allow the ordinal intercept of the relationship(s) between V O 2 total and TNaϩ or GFR to be determined (7,38), or because the data were not presented in a form to allow this relationship to be extracted (29,42,54).…”

Section: Basal Percent Renal V O2mentioning

confidence: 99%

Basal renal O₂consumption and the efficiency of O₂utilization for Na⁺reabsorption

Evans

Harrop

Ngo

et al. 2014

American Journal of Physiology-Renal Physiology

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We examined how the presence of a fixed level of basal renal O2 consumption (Vo2(basal); O2 used for processes independent of Na(+) transport) confounds the utility of the ratio of Na(+) reabsorption (TNa(+)) to total renal Vo2 (Vo2(total)) as an index of the efficiency of O2 utilization for TNa(+). We performed a systematic review and additional experiments in anesthetized rabbits to obtain the best possible estimate of the fractional contribution of Vo2(basal) to Vo2(total) under physiological conditions (basal percent renal Vo2). Estimates of basal percent renal Vo2 from 24 studies varied from 0% to 81.5%. Basal percent renal Vo2 varied with the fractional excretion of Na(+) (FENa(+)) in the 14 studies in which FENa(+) was measured under control conditions. Linear regression analysis predicted a basal percent renal Vo2 of 12.7-16.5% when FENa(+) = 1% (r(2) = 0.48, P = 0.001). Experimentally induced changes in TNa(+) altered TNa(+)/Vo2(total) in a manner consistent with theoretical predictions. We conclude that, because Vo2(basal) represents a significant proportion of Vo2(total), TNa(+)/Vo2(total) can change markedly when TNa(+) itself changes. Therefore, caution should be taken when TNa(+)/Vo2(total) is interpreted as a measure of the efficiency of O2 utilization for TNa(+), particularly under experimental conditions where TNa(+) or Vo2(total) changes.

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“…However, as pointed out (Cafruny B 968), these studies are of little reHevance due to the high doses of mcrcurials administered. Nevertheless, mercurials do reduce kidney tissue oxygen consumption in various preparations (Herms and Kersting 1969;Bowman and Landon 1967;Kessler et al 1964) suggesting that oxidative metabolism is afected during diuresis.…”

Section: Discussionmentioning

confidence: 99%

Organic mercurial diuresis: Inhibition of glutamine utilization in the acidotic rat

Passerini¹,

Welbourne²

1979

Can. J. Physiol. Pharmacol.

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Organic mercurials inhibit mitochondrial glutamine metabolism in vitro while metabolic acidosis, a condition in which the predominant renal fuel is glutamine, potentiates mercurial diuresis. The following studies were undertaken to determine whether potentiation of diuresis reflects mercurial inhibition of glutamine utilization. (1) All three mercurials employed (mersalyl, chlormerodrin, and p-chloromercuribenzoate) are diuretics in the rat and this effect was potentiated by NH4Cl. (2) Despite reabsorbing less sodium, mercurial-treated rats had lower kidney ATP content (4.35 +/- 0.26 and 3.84 +/- 0.43 mumol/g dry weight (mercurial plus NH4Cl) than did controls (4.95 +/- 0.31 and 4.87 +/- 0.39 mumol/g dry weight (NH4Cl). (3) Isolated kidneys from NH4Cl and NH4Cl plus mercurial treated rats were perfused with 1 mM L-[U-14C]glutamine to determine rates of extraction and oxidation. Mercurial-treated acidotic rat kidneys had a reduced rate of glutamine uptake (40.8 +/- 7.4 vs. 64.8 +/- 5.8 mumol/h per kidney), a diminished rate of glutamine conversion to CO2 (14.8 +/- 3.6 vs. 26.4 +/- 5.2 mumol/h per kidney), and a reduction in glucose production (16 +/- 5 vs. 27 +/- 4 mumol/h per kidney). These results are consistent with an effect of organic mercurials upon glutamine utilization, limiting ATP availability, and thereby reducing tubular active sodium reabsorption.

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Effects of Chlormerodrin, p-Chloromercuribenzoate and Dichlorphenamide on Renal Sodium Reabsorption and Oxygen Consumption

Cited by 14 publications

References 8 publications

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

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

Basal renal O₂consumption and the efficiency of O₂utilization for Na⁺reabsorption

Organic mercurial diuresis: Inhibition of glutamine utilization in the acidotic rat

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Effects of Chlormerodrin, p-Chloromercuribenzoate and Dichlorphenamide on Renal Sodium Reabsorption and Oxygen Consumption

Cited by 14 publications

References 8 publications

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

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

Basal renal O2consumption and the efficiency of O2utilization for Na+reabsorption

Organic mercurial diuresis: Inhibition of glutamine utilization in the acidotic rat

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Basal renal O₂consumption and the efficiency of O₂utilization for Na⁺reabsorption