A quantitative analysis of renal ammoniagenesis and energy balance: a theoretical approach

Halperin, Mitchell L.; Jungas, Robert L.; Pichette, Carole; Goldstein, Marc B.

doi:10.1139/y82-212

Cited by 43 publications

(19 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To synthesize NH4+, glutamine is extracted from the glcsmemlar filtrate and the peritubular blood (Lemieux et d. 1974;Pilkington et al 1970). Metabolism s f glutamine to produce NH4+ is a process that yields, ultimately, bicarbonate and ATP as products (Halperin et al 1982). For net gain sf bicarbonate for the body, NH4+ must be made an endproduct of metabolism; this occurs when the cation NH4+ is excreted in the urine (Halperin and Jungas 1983).…”

Section: Discussionmentioning

confidence: 99%

“…1982). Since cells contain such a tiny quantity of the precursor of ATP, ABP, continued flux in pathways that produce ATP can only occur if ATP is reconverted to ADDP (Flatt 1972;Halperin et al 1982;Jungas et al 1992). This occurs in the kidney primarily when sodium is reabsorbed (flux through Na-K ATPase) (Halperin et d. 2982).…”

Section: Discussionmentioning

confidence: 99%

“…Since the production of NH4+ is linked to the extraction of glutamine and the production of ATP (Halperin et al 1982), we were surprised not to find an increased rate of NH4+ production during hypernatrernia (Table 4). In fact, the rates of NH4+ production and glutarnine extraction (per sodium reabsorbed) actually declined (Table 4).…”

Section: Production Of Nh4+mentioning

confidence: 98%

See 2 more Smart Citations

Energy turnover and the production of ammonium by the kidney: effect of hypernatremia

Halperin¹,

Chen²

1992

Can. J. Physiol. Pharmacol.

Self Cite

View full text Add to dashboard Cite

HALPERIN, M. L., and CHEN, C.-B. 1992. Energy turnover and the production of ammonium by the kidney: effect of hypernatremia. Can. J. Physiol. Pharmacol. 70: 8 -12.The pupsse of this study was to explore further the relation between the rates of oxygen consumption and ammonium (NH,+) production in the kidney during chronic metabolic acidosis. The experimental model was the dog with chronic metabolic acidosis because of the extensive background literature in this species. Chronic metabolic acidosis was produced by h e ingestion of 10 mmol NH,CI/kg body weight for 5 days. There was a significant increase in the rate of oxygen extraction when hyprnatremia was present. Despite this rise in the rate of oxygen consumption, there was no increase in the rate of NH4+ production nor in the rate of glutamine extraction. These data suggest that hyprnatremia might prevent a further augmentation in glutamine extraction when the rate of oxygen consumption rises. In addition, a larger proportion of the NM,+ produced was excreted in the urine during hypernatremia. This increase was associated with a rise in the urine flow rate, but not with a fall in urine pH.Key words: Acid -base, ATP, glutamine, energy metabolism, metabolic acidosis, metabolic regulation, nee acid excretion, oxygen consumption. During chronic metabolic acidosis, the expected renal response is to generate new bicarbonate; this is accomplished rnahly by the production and excretion of TWO major steps are involved: first, glutamine is metabolized in cells of the proximal tubule, yielding NH4+ and bicarbonate as products (Halperin et al. 1991); second, the cation, NH4+, must be transferred to the urine (Knepper et d. 1989)* During the metabolism sf glutamiwe to either glucose or C 0 2 , ATP is produced (Hdperiw et al. 1982). Hence the rate of turnover of energy (ATP) could limit the synthesis of N h f in these cells because no organ or organelle can synthesize ATP at a rate that exceeds its rate of utilization even for 1 min, owing to the very small quantity of ADP in cells (Hllatt 1972; Hdperin et al. 1985b; Hdperin et al. 1982; Jungas et d. 1992). Since at least 90% sf the ATP turnover in the kidney appears to be related to sodium reabsorption (Mandel and Balaban 198 I), owe might anticipate that a direct relationship exists between the rates of oxygen consumption and gllutarnine oxidation (Halperin et daB. 1985). Two exceptions to this rule have been observed in dogs with chronic metabolic acidosis. 1976)) were infbased and oxidized, ATP was produced without the synthesis sf NH4+. Now there was a substantial (and pre-'Author for correspondence.Printcd rn Canada i Imprime au Canada dictable) decline in the rate of NH4+ pr~duction. Second, during acute hyponatremia, the rate of oxygen consumption rose, but no extra glgltamine was extracted. In this setting, there was complete oxidation and ns transamination of glutamine (Hdprin md Chen 1990), presumably reflecting increased oxidation s f alanine.To explore the relationship between the consumption of oxygen and ...

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Energy turnover and the production of ammonium by the kidney: effect of hypernatremia

Halperin¹,

Chen²

1992

Can. J. Physiol. Pharmacol.

Self Cite

View full text Add to dashboard Cite

show abstract

“…The rate of oxidation of β-HB – or glutamine (production of NH 4 + ) by the kidney depends on the rate of generation of ADP in that organ [16]. ADP is generated when ATP is used to perform renal work (reabsorbing filtered Na + , fig.…”

Section: Concept 1: H+ Are Added To the Body When There Is A Net Incrmentioning

confidence: 99%

A Conceptual Approach to the Patient with Metabolic Acidosis

Shafiee

Kamel²,

Halperin³

2002

Nephron

Self Cite

View full text Add to dashboard Cite

We shall illustrate that management of patients with an acid-base disorder could be improved if the acid-base analysis was based on a better understanding of basic concepts of physiology. Three concepts of acid-base physiology and their clinical implications are emphasized in a patient with diabetic ketoacidosis. First, when an acid is produced from neutral precursors in the body, there is a net increase in the number of hydrogen ions (H⁺) and new anions. The corollary is that H⁺ will be removed when the accompanying anion is metabolized to a neutral end-product or is excreted in the urine with H⁺ or ammonium (NH₄⁺). Second, buffering of H⁺ is beneficial if H⁺ are removed by bicarbonate rather than being able to bind to proteins. This latter function depends on having a low tissue PCO₂, due to a combination of hyperventilation plus an adequate blood flow rate to vital organs. Third, the kidneys add new bicarbonate to the body when NH₄⁺ is excreted with chloride ions.

show abstract

“…Several authors have demonstrated that glutamine may be converted into glucose and C02 by rat proximal tubules or slices in vitro (Kamm & Strope, 1972;Baverel & Lund, 1979;Watford et al 1980;Baverel et al 1984). The net provision of energy during glutamine metabolism results from both complete oxidation of its carbon skeleton and, to a lesser extent, gluconeogenesis (Halperin et al 1982). Therefore, irrespective of the relative importance of complete oxidation and glucose synthesis from glutamine, this amino acid appears to be an energy supplier to the proximal tubule of fed rats.…”

Section: Adaptative Changes In Fuel Selection By the Rat Kidney Durinmentioning

confidence: 99%

Fuel selection by the kidney: adaptation to starvation

1995

View full text Add to dashboard Cite

A quantitative analysis of renal ammoniagenesis and energy balance: a theoretical approach

Cited by 43 publications

References 5 publications

Energy turnover and the production of ammonium by the kidney: effect of hypernatremia

Energy turnover and the production of ammonium by the kidney: effect of hypernatremia

A Conceptual Approach to the Patient with Metabolic Acidosis

Fuel selection by the kidney: adaptation to starvation

Contact Info

Product

Resources

About