Renal Ammonia Production and Excretion

Tannen, Richard L.

doi:10.1002/cphy.cp080123

Cited by 10 publications

(3 citation statements)

References 306 publications

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“…The increased renal synthesis of ammonium and bicarbonate ions from plasma glutamine is an essential compensatory response to the onset of metabolic acidosis (1). Increased renal excretion of ammonium ions provides an expendable cation that facilitates the excretion of acids while conserving sodium and potassium ions (2). In contrast, the resulting bicarbonate ions are selectively transported across the basolateral membrane to compensate partially for the decrease in plasma pH and bicarbonate ions (3).…”

mentioning

confidence: 99%

Effect of Acidosis on the Properties of the Glutaminase mRNA pH-Response Element Binding Protein

Laterza¹,

Curthoys²

2000

Journal of the American Society of Nephrology

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Abstract. The pH-responsive stabilization of the rat renal glutaminase (GA) mRNA during metabolic acidosis is mediated by a pH-response element (pH-RE). The primary pH-RE within the GA mRNA consists of a direct repeat of an 8-base adenosine and uridine—rich sequence, which binds a specific cytosolic protein, the pH-response element binding protein (REBP). The functional analysis of this system was performed in LLC-PK1-F+ cells, a pH-responsive line of porcine proximal tubule-like cells. Cytosolic extracts of LLC-PK1-F+ cells also contain a protein that binds with high affinity to the rat GA mRNA pH-RE. The apparent binding of this protein is increased threefold in cytosolic extracts prepared from LLC-PK1-F+ cells that were grown in acidic medium (pH = 6.9, HCO3- = 10 mM). Extracts prepared from the renal cortext of rats that were made acutely acidotic also exhibit a similar increase in binding to the RNA probe that contains the direct repeat of the pH-RE. The temporal increase in binding correlates with the temporal increase in GA mRNA. Scatchard analysis indicates that the increased binding is due to an increase in both the affinity and the maximal binding of the pH-REBP. Thus, increased binding of the pH-REBP to the GA mRNA may initiate its stabilization and increased expression during acidosis.

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mentioning

confidence: 99%

Effect of Acidosis on the Properties of the Glutaminase mRNA pH-Response Element Binding Protein

Laterza¹,

Curthoys²

2000

Journal of the American Society of Nephrology

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“…However, it is firmly established that chronic metabolic acidosis increases renal capacity to produce ammonia. This has been readily demonstrated in the rat, dog, and human both in vivo and in vitro studies (Tannen, ). Although low pH may play a direct role, other factors including increased activity of enzymes involved in glutamine deamination and metabolism such as phosphoenolpyruvate carboxykinase (PEPCK) and phosphate‐dependent glutaminase (PDG) have been demonstrated (Tannen, ).…”

Section: Discussionmentioning

confidence: 85%

Effects of chronic hypercapnia on ammonium transport in the mouse kidney

et al. 2019

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Hypercapnia and subsequent respiratory acidosis are serious complications in many patients with respiratory disorders. The acute response to hypercapnia is buffering of H + by hemoglobin and cellular proteins but this effect is limited. The chronic response is renal compensation that increases HCO 3 − reabsorption, and stimulates urinary excretion of titratable acids (TA) and NH 4 + . However, the main effective pathway is the excretion of NH 4 + in the collecting duct. Our hypothesis is that, the renal NH 3 /NH 4 + transporters, Rhbg and Rhcg, in the collecting duct mediate this response. The effect of hypercapnia on these transporters is unknown. We conducted in vivo experiments on mice subjected to chronic hypercapnia. One group breathed 8% CO 2 and the other breathed normal air as control (0.04% CO 2 ). After 3 days, the mice were euthanized and kidneys, blood, and urine samples were collected. We used immunohistochemistry and Western blot analysis to determine the effects of high CO 2 on localization and expression of the Rh proteins, carbonic anhydrase IV, and pendrin. In hypercapnic animals, there was a significant increase in urinary NH 4 + excretion but no change in TA. Western blot analysis showed a significant increase in cortical expression of Rhbg (43%) but not of Rhcg. Expression of CA‐IV was increased but pendrin was reduced. These data suggest that hypercapnia leads to compensatory upregulation of Rhbg that contributes to excretion of NH 3 /NH 4 + in the kidney. These studies are the first to show a link among hypercapnia, NH 4 + excretion, and Rh expression.

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“…The kidneys harbor gluconeogenic and ammoniagenic enzymes responsive to acid-base and substrate influences (127). Most of the glucose released from the liver and kidney is derived from recycled lactate, pyruvate and alanine (35,80), from glycerol released from triglycerides (80,84), from acetone derived from decarboxylated AcAc- (110), and from glutamine released by muscle (68,77), brain (47) and other proteinaceous sources (77).…”

Section: Gluconeogenesis Ketogenesis Ureagenesis Ammoniagenesis Anmentioning

confidence: 99%

Starvation

Owen¹,

Smalley²,

Jungas³

2001

Comprehensive Physiology

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The sections in this article are: Fundamental Principles and Observations of Bioenergetics Epidemiology Weight Loss, Body Composition and Energy Requirements During Food Deprivation Urinary Excretory Products During Total Starvation General Metabolism During Starvation Anaplerosis and Cataplerosis Gluconeogenesis, Ketogenesis, Ureagenesis, Ammoniagenesis and Acid‐Base Balance Minimum Protein, Fat and Glucose Requirements Endocrine Signals Insulin Glucagon Catecholamines lodothyronines Growth Hormone, Insulin‐like Growth Factor and Cortisol Leptin and Neuroendocrine Factors Clinical Observations

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Renal Ammonia Production and Excretion

Cited by 10 publications

References 306 publications

Effect of Acidosis on the Properties of the Glutaminase mRNA pH-Response Element Binding Protein

Effect of Acidosis on the Properties of the Glutaminase mRNA pH-Response Element Binding Protein

Effects of chronic hypercapnia on ammonium transport in the mouse kidney

Starvation

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