Renal Hemodynamics and Ammoniagenesis

Lemieux, Guy; Vinay, Patrick; Cartier, P

doi:10.1172/jci107629

Cited by 36 publications

(4 citation statements)

References 22 publications

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“…The difference in the total ammonia production between tubules perfused with glutamine and tubules perfused without glutamine suggests that the delivery of glutamine, the main substrate for ammonia production (19,20), to the tubular lumen directly enhances total ammonia production. Such data are consistent with observations made in the intact dog, which indicate that glutamine filtered at the glomerulus and reabsorbed along the nephron accounts for a major portion of renal glutamine extraction and that glutamine extraction is proportional to ammonia production (21). Even in the absence of glutamine in the perfusate, the rate of total ammonia production was greater in perfused segments compared with unperfused segments.…”

Section: Resultssupporting

confidence: 91%

Regulation of ammonia production by mouse proximal tubules perfused in vitro. Effect of luminal perfusion.

Nagami¹,

Kurokawa²

1985

J. Clin. Invest.

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To investigate factors regulating ammonia (NH3) production by isolated defined proximal tubule segments, we examined the rates of total NH3 (NH3 + NH') production by individual proximal tubule segments perfused in vitro under a variety of perfusion conditions. Segments consisting of late convoluted and early straight portions of superficial proximal tubules were incubated at 370C in Krebs-Ringer bicarbonate (KRB) buffer containing 0.5 mM L-glutamine and 1.0 mM sodium acetate, pH 7.4. The rate of total ammonia production was calculated from the rate of accumulation of total NH3 in the bath. The total ammonia production rate by unperfused proximal segments was 6.0±0.2 (±SE) pmol/mm per minute, which was significantly lower than segments perfused at a flow rate of 22.7±3.4 nl/min with KRB buffer (21.5±1.4 pmol/mm per minute; P < 0.001) or with KRB buffer containing 0.5 mM L-glutamine (31.9±2.5; P < 0.001). The rate of NH3 production was higher in segments perfused with glutamine than in segments perfused without glutamine (P < 0.01).The perfusion-associated stimulation of NH3 production was characterized further. Analysis of collected luminal fluid samples revealed that the luminal fluid total NH3 leaving the distal end of the perfused proximal segment accounted for 91% of the increment in NH3 production observed with perfusion. Increasing the perfusion flow rate from 3.7±0.1 to 22.7±3.4 nl/min by raising the perfusion pressure resulted in an increased rate of total NH3 production in the presence or absence of perfusate glutamine (mean rise in rate of total NH3 production was 14.9±3.7 pmol/mm per minute in segments perfused with glutamine and 7.8±0.9 in those perfused without glutamine). In addition, increasing the perfusion flow rate at a constant perfusion pressure increased the rate of luminal output of NH3. Total NH3 production was not affected by reducing perfusate sodium concentration to 25 mM and adding 1.0 mM amiloride to the perfusate, a condition that was shown to inhibit proximal tubule fluid reabsorption. These observations demonstrate that the rate of total NH3 production by the mouse proximal tubule is accelerated by perfusion of the lumen of the segment, by the presence of glutamine in the perfusate,

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Section: Resultssupporting

confidence: 91%

Regulation of ammonia production by mouse proximal tubules perfused in vitro. Effect of luminal perfusion.

Nagami¹,

Kurokawa²

1985

J. Clin. Invest.

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“…The independence of the PG effects from renal hemodynamic changes is strengthened by the fact that inhibitors of PG synthesis stimulate ammonia production but tend to reduce RBF and GFR (20). The latter effect ought to diminish, not enhance, ammoniagenesis (21). While the PG-ammonia effect clearly takes place in the cortex, we have yet to identify the exact anatomic site of this interaction.…”

Section: Discussionmentioning

confidence: 98%

Prostaglandins inhibit renal ammoniagenesis in the rat.

Jones¹,

Beck²,

Kapoor³

et al. 1984

J. Clin. Invest.

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Abstract. We describe the inhibitory effect of prostaglandins (PGs) on in vivo rat renal ammonia synthesis. The influence of systemic pH upon urinary PG excretion and ammoniagenesis was also investigated. Finally, PG production by incubated rat renal cortical slices was suppressed to investigate the PG-ammonia interplay in the absence of changes in renal blood flow, glomerular filtration rate, ambient electrolyte concentrations or extrarenal hormonal factors.In vivo ammonia synthesis doubled and PG excretion fell by 44% in normal rats, after intravenous administration of 1 mg/kg of meclofenamate. Higher doses of meclofenamate further augmented ammonia production and further reduced PG excretion. PG depletion was also associated with an increase in fractional excretion of ammonia (FENH3) that was independent of changes in urine flow rate or pH.Acute metabolic acidosis (AMA) increased total ammonia synthesis but also stimulated PG production. Administration of meclofenamate to rats with mild AMA markedly reduced urinary PG excretion, further augmented ammonia synthesis, and significantly increased the FENH3. Inhibition of stimulated PG synthesis during severe AMA did not increase ammoniagenesis or FENH3. Acute metabolic alkalosis did not alter production of PGs or ammonia, but reduced the FENH3 by A preliminary abstract was presented at

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“…was postulated to be related to glutamine transport. No effects were found on the tubular and peritubular transport rates of glutamine when studied either in vivo (21) or in isolated membrane vesicles (35). Isolated renal cortical mitochondria, on the other händ, exhibited a mafked HCO^ dependence in their transport propert ies for glutamate (36) ?…”

Section: Regulation Of Renal Ammoniagenesis and Ammonium Transportmentioning

confidence: 99%

Renal and Hepatic Nitrogen Metabolism in Systemic Acid Base Regulation

Guder

Häussinger²,

Gerok³

1987

Clinical Chemistry and Laboratory Medicine

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Summary:Renal and hepatic nitrogen metabolism are linked by an interorgan glutamine flux, coupling both renal ammoniagenesis and hepatic urea production to systemic acid-base regulation. Reconsideration of established pathways and recent observations led to a conceptional change with a movement from a twoorgan concept (lungs and kidney) of acid-base balance to a three-or-more organ concept (lungs, kidney, liver). This development implies new regulatory sites of systemic pH control and consequently a new pathophysiological understanding of derangements of acid-base homeostasis.In this new concept the urea cycle regulates the removal of metabolically generated bicarbonate during a protein load in a pH-and bicarbonate-dependent manner. This is related to a switch of hepatic ammonium detoxication from urea to glutamine synthesis in metabolic acidpsis, and vice versa in alkalosis. An adaptive increase in the renal capacity for glutamine deamidation and deamination and for ammonium excretion leads to a proportional decrease in renal urea excretion at the expense of ammonium in acidotic conditions.

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Renal Hemodynamics and Ammoniagenesis

Cited by 36 publications

References 22 publications

Regulation of ammonia production by mouse proximal tubules perfused in vitro. Effect of luminal perfusion.

Regulation of ammonia production by mouse proximal tubules perfused in vitro. Effect of luminal perfusion.

Prostaglandins inhibit renal ammoniagenesis in the rat.

Renal and Hepatic Nitrogen Metabolism in Systemic Acid Base Regulation

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