Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rate of net glutamine degradation in non-recirculating perfused rat liver was estimated by the release of urea, ammonia and alanine in steady states of operation of glutaminase. Corrected for a slight intracellular accumulation of glutamate, accounting for 7% of the flux at 5mM glutamine, the estimated glutaminase activity agrees well with measurements of glutamine removal described in the literature for recirculating perfusion experiments. Glutaminase activity was decreased when the perfusate pH was lowered (i) by infusion of hydrochloric acid, (ii) by increasing the CO2 concentration, or (iii) by decreasing the hydrogencarbonate concentration. Conversely, it was increased when the perfusate pH was increased by infusion of sodium hydroxide or by increasing the hydrogencarbonate concentration. However, glutaminase activity did not depend on medium hydrogencarbonate. When the hydrogencarbonate buffer system was replaced by DMO or by Hepes equilibrated with O2 (no CO2 present), there was practically no change in the observed rates. These results, obtained in an iso-pH system, are in contrast to recent suggestions of a role of hydrogencarbonate in the regulation of glutamine metabolism based on results from incubations of isolated mitochondria or hepatocytes. It is concluded that the conservation of glutamine by the inhibition of hepatic glutaminase, which provides glutamine for the pH regulation by renal glutaminase, can be increased not only in metabolic acidosis but also in respiratory acidosis associated with high hydrogencarbonate concentration.
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PMID:The role of pH and the lack of a requirement for hydorgencarbonate in the regulation of hepatic glutamine metabolism. 740 50

Experiments on rats have shown an important role of hypercapnia in the development of condition of artificial hibernation in combination with influence of hypothermia, hypoxia and hypercapnia. It is proved that the joint action of hypothermia, hypoxia and hypercapnia has induced development of respiratory acidosis and hibernation in animals, while removal of the hypercapnia effect has induced development of acute metabolic acidosis and death of animals. It has been found that animals in the state of artificial hibernation have considerable changes in concentrations of main electrolytes (Na+, K+, Ca+, Mg2+, phosphates, Cl-) and metabolites (NH3, glutamine, urea) in blood as well as in activity of enzymes (glutamaldehydrogenase, glutaminase, arginase) in tissues of the liver and kidneys.
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PMID:[Acid-base equilibrium and nitrogen metabolism in rats in a state of artificial hibernation]. 855 76

The role of extracellular glutamate formation as opposed to cellular glutamate removal in regulating monolayer glutamate content in response to metabolic acidosis was studied in LLC-PK1-F+ cells. Exposure to metabolic acidosis (14 mM bicarbonate; pH 7.1) for 18 h resulted in 24% fall in monolayer glutamate content. Of this, approximately one-half could be attributed to enhanced glutamate removal via glutamate dehydrogenase, consistent with a rise in ammonium production. The remainder appears due to reduced extracellular glutamate formation as a consequence of diminished gamma-glutamyltranspeptidase (gamma-Gt) activity. Metabolic acidosis, but not respiratory acidosis, resulted in a 33% fall in gamma-Gt activity and a proportional fall in extracellular glutamate formation; glutamate transport into these cells was not rate limiting in acidosis. Overall glutamine utilization decreased 36%, reflecting the fall in gamma-Gt activity as well as a decrease in a pH-sensitive glutamine uptake, whereas glutamine transport coupled to the phosphate-dependent glutaminase flux increased. It is noteworthy that the increased ammonium produced in metabolic acidosis was preferentially secreted into the apical compartment; acid secretion, but not production, was similarly increased. Thus reduced cellular glutamate appears to coordinate activation of intracellular glutaminase to the apical membrane exchanger, consistent with the functioning kidney response to metabolic acidosis.
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PMID:Response of LLC-PK1-F+ cells to metabolic acidosis. 863 75