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PubMed2003

Effect of acute acidosis on protein and amino acid metabolism in rats.

BACKGROUND & AIMS: Metabolic acidosis is a common finding in critical illness. The aim of the present study was to evaluate acute acidosis as a signal that induces changes in protein metabolism. METHODS: In the first study, Wistar rats were infused for 6h with HCl or saline resulting in blood pH7.30+/-0.03 and 7.46+/-0.02, respectively. The whole body protein metabolism was evaluated using L-[1-(14)C]leucine. In the second study, soleus and extensor digitorum longus muscles from normal rats were incubated in medium, pH7.4, 7.3 or 7.0. Protein metabolism was evaluated using L-[1-(14)C]leucine and tyrosine release. RESULTS: In the in vivo study we observed increased protein turnover-protein synthesis, proteolysis and leucine oxidation and more negative protein balance in rats with acidosis. There was no change in protein synthesis in gastrocnemius muscle. We observed an increase in plasma levels of most amino acids including branched-chain amino acids and a decrease in intracellular amino acid pool in skeletal muscle. In vitro decrease in pH of 0.1 had no effect on protein metabolism, decrease of 0.4 decreased protein turnover and leucine oxidation. CONCLUSION: Acute metabolic acidosis is a protein wasting condition. Direct effect of acidosis on skeletal muscle is under condition in vivo modified by neurohumoral regulations.

Acidosis↗
PubMed1992

Should the urine PCO2 or the rate of excretion of ammonium be the gold standard to diagnose distal renal tubular acidosis?

A high rate of excretion of ammonium (NH4+) during chronic metabolic acidosis should rule out the diagnosis of distal renal tubular acidosis (RTA). Bearing this in mind, the purpose of this report is to demonstrate that a low urine minus blood PCO2 difference in alkaline urine (U-B PCO2) is a less reliable indicator of the diagnosis of distal RTA. The patient who is the subject of this report sniffs glue on a chronic, but intermittent basis. He presented with metabolic acidosis (pH 7.20; bicarbonate, 10 mmol/L) and an anion gap in plasma of 20 mEq/L. The urine anion gap (-14 mEq/L) and osmolal gap (185 mmol/L [mOsm/kg] H2O) suggested that there was a high, rather than a low, rate of excretion of NH4+. This was confirmed by direct measurement of NH4+ in the urine (101 mumol/min). The high rate of excretion of NH4+ suggested that the metabolic acidosis was due, in large part, to an abnormally high rate of production of acid (hippuric acid, because the rate of excretion of hippurate was 76 mumol/min). The U-B PCO2 was low (10 mm Hg) on the second hospital day, after the acidosis was corrected. Potential reasons for the discrepancy between the high rate of excretion of NH4+ and the low U-B PCO2 are discussed.

Acidosis, Renal Tubular↗
PubMed1999

Metabolic acidosis in advanced renal failure: differences between diabetic and nondiabetic patients.

Metabolic acidosis is almost invariably a consequence of advanced renal failure, although its severity can vary widely. To evaluate the determinants of the severity of metabolic acidosis, with special interest in determining if there is any difference in the prevalence and severity of metabolic acidosis between patients with and without diabetes, 113 predialysis patients with renal failure were studied. Criteria for inclusion onto the study were: creatinine clearance (Ccr)/1.73 m2 less than 30 mL/min, no alkali therapy within the previous 30 days, and the absence of respiratory diseases. Forty-eight patients had diabetes (33 patients with diabetic nephropathy). The following data were analyzed: demographics; cause of renal failure; hematocrit; serum urea, creatinine, uric acid, albumin, glucose, hemoglobin A1c, bicarbonate, sodium, potassium, chloride, calcium, phosphorus, and alkaline phosphatase levels; anion gap; urinary protein excretion; Ccr/1.73 m2; half of the sum of creatinine and urea clearances (Ccr-Cu); protein-equivalent nitrogen appearance (PNA); and whether the patients received diuretics (75 patients), angiotensin-converting enzyme inhibitors (54 patients), and/or calcium channel blockers (55 patients). After the exclusion of eight patients because of hypochloremia (three patients with and five patients without diabetes), mean serum bicarbonate levels were significantly greater in patients with diabetes than in the rest of the patients (20.7 +/- 2.3 v 18.2 +/- 2. 3 mmol/L; P = 0.0001). The mean anion gap (mmol/L) was also significantly less in patients with than without diabetes (19.70 +/- 3.65 v 22.35 +/- 3.64; P = 0.003). Eleven of 105 patients had serum bicarbonate levels of 23 mmol/L or greater (9 patients with and 2 patients without diabetes). Pure elevated anion gap followed by mixed (high anion gap and hyperchloremia) were the most common types of metabolic acidosis observed in both groups. There were no differences in PNA, diuretic treatment, or vomiting history between patients with and without diabetes. By multiple logistic regression analysis, the best determinants for a serum bicarbonate level greater than 19 mmol/L were: the diagnosis of diabetic nephropathy (odds ratio, 0.107; P = 0.0002), Ccr-Cu (odds ratio, 0.824; P = 0. 014), and age (odds ratio, 0.966; P = 0.046). In conclusion, patients with diabetes with advanced renal failure showed a less severe metabolic acidosis, which cannot be explained by gastrointestinal hydrogen ion losses, drugs, or reduced protein catabolic rate. Patients with diabetes may have a more efficient extrarenal generation of bicarbonate than end-stage renal failure patients without diabetes.

Acidosis, Renal Tubular↗
PubMed1997

Neuronal injury in experimental status epilepticus in the rat: role of acidosis.

Systemic and cerebral acidosis accompanies generalized tonic-clonic seizures and status epilepticus. Acidosis during status may be modified by neuromuscular paralysis, intubation and ventilation, or administration of a base, but the effect of acidosis on neuronal injury from status is uncertain. We studied the effect of acidosis, induced by hypercarbic ventilation, on heat-shock protein (HSP72) induction in rat brain as a measure of neuronal injury in experimental status epilepticus. Acidosis was found to attenuate neuronal injury, independent of its anticonvulsant effect.

Acidosis↗
PubMed1998

Intraplantar injection of hyaluronic acid at low pH into the rat hindpaw produces tissue acidosis and enhances withdrawal responses to mechanical stimuli.

Application of buffers covering a range of acidic pH values activates and sensitizes nociceptors and produces pain. The purpose of this study was to determine whether a range of acidic pH in tissue produces mechanical hyperalgesia. Tissue acidosis was produced in the hindpaw of the rat by intraplantar injections of hyaluronic acid (HA) adjusted to pH 7.4, 6.0, 5.0, 4.0 or 3.0. Mechanical hyperalgesia was assessed by evaluating responses to application of a von Frey monofilament to the plantar surface before and after injection of HA. In separate experiments, magnitude of tissue acidosis produced by injection of HA was determined by measuring pH of intraplantar tissue using a pH microelectrode. Although needle stick alone produced mechanical hyperalgesia, intraplantar injections of HA at pH 6.0 or 5.0 produced significantly greater mechanical hyperalgesia. In contrast, mechanical hyperalgesia produced by injection of HA at pH 7.4, 4.0 or 3.0 was not different from that produced by needle stick. Although injection of HA at low pH produced tissue acidosis in a pH dependent manner, only a narrow range of tissue acidosis (pH = 6.38-6.00) produced mechanical hyperalgesia. Our data suggest that tissue acidosis induces mechanical hyperalgesia; however, the range of tissue pH that produces this effect is limited.

Acidosis↗
PubMedDate not supplied

Phenformin and lactic acidosis: a case report and review.

Phenformin was removed from the U.S. market 20 years ago because of a high incidence of lactic acidosis. Unfortunately, this medication is still available from foreign sources. Another biguanide, metformin, was reintroduced to the United States market for the treatment of diabetes. Biguanide-induced lactic acidosis should be included in the differential diagnosis of elevated anion gap metabolic acidosis. We present a case of phenformin-induced lactic acidosis in which we were consulted at the local poison control center. We also review its pathophysiology, presentation, and treatment. A review of the actions of phenformin illustrates the mechanism of pathology that may also occur with metformin. Risk factors for the development of lactic acidosis include renal deficiency, hepatic disease, cardiac disease, and drug interaction such as cimetidine.

Acidosis, Lactic↗
PubMed1997

Clinical and biochemical aspects of thiamine treatment for metabolic acidosis during total parenteral nutrition.

We encountered six cases of total parenteral nutrition (TPN)-associated lactic acidosis during the 6-y period of 1988-1993. The patients were characterized by severe disease of the digestive organs, minimal food intake before surgery, and postoperative TPN with no food intake and with no vitamin supplements. Within 4 wk of TPN, they developed hypotension (< or = 80/60 mmHg), Kussmaul's respiration, and clouding of consciousness, as well as abdominal pain not directly related to the underlying disease. Routine laboratory examinations revealed no acute aggravation in hepatic, renal, or pancreatic functions. Arterial blood gas analysis showed pH < or = 7.134 and base excess < or = -17.5 mmol/L. Additional laboratory examinations revealed serum lactate > or = 10.9 mmol/L, serum pyruvate > or = 159 mumol/L, and lactate/pyruvate ratio > or = 0.029. None of the patients responded to sodium bicarbonate or other conventional emergency treatments for shock and lactic acidosis. After the first case, we suspected that thiamine deficiency might be responsible for this pathologic condition, Serum thiamine was proved to be < or = 196 nmol/L in 5 patients. Thiamine replenishment at intravenous doses of 100 mg every 12 h resolved lactic acidosis and improved the clinical condition in 3 patients. This article includes a review of 11 relevant reports published from 1982-1992 and a discussion of the biochemical mechanism of onset of thiamine deficiency-associated lactic acidosis. We emphasize the needs (1) to supplement TPN with thiamine-containing vitamins for the patients whose food intake does not meet nutritional requirements; (2) to monitor the patients routinely measuring serum thiamine concentration and erythrocyte transketolase activity during TPN; and (3) to intravenously replenish using high-dose thiamine simultaneously with the manifestation of signs and symptoms of lactic acidosis.

Acidosis, Lactic↗
PubMed2003

Renal tubular acidosis secondary to FK506 in living donor liver transplantation: a case report.

FK506 is an immunosuppressant that is thought to be less nephrotoxic than cyclosporine A. However, complications due to renal tubular acidosis (RTA) have recently been reported. We report a case of RTA secondary to FK506 administration in liver transplantation. A 6-month-old girl was treated with FK506 after undergoing living donor liver transplantation for fulminant hepatitis. On postoperative day 17, she demonstrated hyperkalaemia and metabolic acidosis; she was diagnosed to have hyperkalaemic distal RTA with aldosterone deficiency (type IV). Intravenous sodium bicarbonate and furosemide, and intrarectal calcium polystyrenesulfonate were administered to correct the acidosis and promote potassium secretion. Thereafter, the FK506 concentration in whole blood gradually decreased, and the hyperkalaemia and metabolic acidosis following RTA improved. RTA is one type of nephrotoxicity induced by FK506, and it is reversible in mild cases when appropriately treated. The mechanism of RTA induced by FK506 has not yet been clearly elucidated. Surgeons and physicians should therefore be aware of the potential for RTA to occur with FK506 after any organ transplantation. The treatment for acidosis and hyperkalaemia should be started as soon as RTA is diagnosed, and the dosage of FK506 should also be reduced if possible.

Acidosis, Renal Tubular↗
PubMed2000

Branchial chemoreceptors mediate ventilatory responses to hypercapnic acidosis in channel catfish.

The effects of hyperoxic hypercapnia on cardiovascular and ventilatory variables and blood gas and acid/base parameters were examined in conscious and anesthetized spontaneously breathing (ASB) channel catfish, Ictalurus punctatus. These separate experiments were designed to determine: (1) if channel catfish show a ventilatory response to hypercapnic acidosis when blood O(2) content is maintained in conscious animals; and (2) whether branchial receptors innervated by cranial nerves IX and X mediate this response. The combination of high O(2) and CO(2) tensions allowed the cardioventilatory effects of hypercapnic acidosis to be assessed independently of Root or Bohr mediated changes in blood O(2) content. In the absence of significant changes in dorsal or ventral aorta O(2) content, hyperoxic hypercapnia significantly stimulated ventilation, relative to hyperoxic exposure. Hypercapnic acidosis, however, had no significant effects on blood pressure or heart rate. Branchial denervation in ASB fish abolished the ventilatory response to hypercapnic acidosis. The results indicate that hypercapnic acidosis independently stimulates ventilation in channel catfish. This response is mediated by CO(2)/pH-sensitive branchial receptors innervated by cranial nerves IX and X.

Acidosis↗
PubMed1991

Mechanism of altered renal glutaminase gene expression in response to chronic acidosis.

Increased rat renal ammoniagenesis is sustained during chronic metabolic acidosis by the cell-specific induction of the regulatory enzymes of glutamine catabolism and of gluconeogenesis. A glutaminase-specific cDNA hybridizes to 6.0- and 3.4-kb mRNAs that are contained in total or poly(A)+ RNA isolated from rat kidney. When translated in a rabbit reticulocyte lysate, each of the fractionated mRNAs produces the 72-kDa precursor of the mitochondrial glutaminase. The levels of both mRNAs are increased 5-fold within 1 day following onset of chronic acidosis and reach a maximum (8-fold) after 5 days. During recovery from chronic acidosis, the levels of the glutaminase mRNAs are returned to normal within 1 day. The observed changes in mRNA levels correlate with equivalent changes in the relative levels of translatable glutaminase mRNA. Nuclear run-on assays indicate that the rate of transcription of the renal phosphoenolpyruvate carboxykinase gene is increased and decreased in response to onset and recovery from chronic acidosis, respectively. In contrast, the rates of transcription of the glutaminase and beta-actin genes are unaffected by alterations in acid-base balance. Thus, the increase in renal glutaminase activity during chronic acidosis results from an equivalent increase in the levels of total and translatable glutaminase mRNAs which apparently results from an increased stability of the glutaminase mRNA.

Acidosis↗
PubMed1982

Parathyroid hormone is not anticalciuric during chronic metabolic acidosis.

The role of parathyroid hormone (PTH) on calcium excretion during chronic metabolic acidosis was investigated in intact and thyroparathyroidectomized (TPTX) acidotic and control dogs. Intact dogs fed NH4Cl for 3 days developed marked hypercalciuria as compared to intact control animals. After thyroparathyroidectomy, calcium excretion corrected per glomerular filtration rate decreased significantly in NH4Cl-treated dogs but not in the controls. This was observed in the face of a TPTX-induced fall in filtered load of calcium in both groups. After restoration of filtered load of calcium to normal by CaCl2 infusion, fractional calcium excretion at any level of fractional sodium excretion was higher in NH4Cl-treated TPTX dogs than that of TPTX controls, indicating a calciuric effect of acidosis independent of PTH. PtH (1 U/min X 60 min) was infused to examine the effect of this hormone on calcium excretion during NH4Cl-induced acidosis. In normal dogs, PTH significantly decreased absolute and fractional calcium excretion. In contrast, PTH infusion to acidotic dogs failed to decrease absolute and fractional calcium excretion. In both groups, phosphate excretion increased significantly. The higher calcium excretion of acidotic dogs during PTH infusion resulted from failure to enhance calcium reabsorption as shown by the fact that, at any level of plasma ionizable calcium, calcium excretion was higher in acidotic dogs than in controls. These findings indicate that during metabolic acidosis PTH does not exert its normal anticalciuric effect. This may contribute to the development of hypercalciuria despite PTH excess in certain clinical conditions associated with chronic metabolic acidosis.

Acidosis↗
PubMed1984

Hypophosphaturia impairs the renal defense against metabolic acidosis.

It is known that Pi normally provides the major source of non-NH3 urinary buffer and that Pi-buffered renal H+ excretion (titratable acidity, TA) accounts for a large fraction of daily renal net acid excretion (NAE). Whether the presence of luminal non-NH3 buffers is a prerequisite to normal renal regulation of systemic acid-base equilibrium under any conditions has not been investigated. Accordingly, I investigated whether chronic renal regulation of plasma (p) [HCO3] might be impaired under conditions of normophosphatemic hypophosphaturia (NHP) produced by short-term dietary Pi restriction. During a steady-state of HCl-induced acidosis in NaCl-replete NHP dogs (group 1A, N = 6), [HCO3-]p averaged 14.1 +/- 0.6 mEq/liter and arterial (a) [H+] averaged 54 +/- 2 nEq/liter. Substitution K+ 2.5 mEq/kg as neutral Pi for equivalent dietary KCl for 7 to 8 days resulted in significant amelioration of acidosis (delta [HCO3-]p + 2.2 +/- 0.5 mEq/liter, P less than 0.01; delta [H+]a -6 +/- 2 nEq/liter, P less than 0.01) in association with a cumulative increment (sigma delta) in TA excretion (+ 103 mEq, P less than 0.001) and NAE (+ 22 mEq). To investigate whether Pi-induced amelioration of acidosis was related to enhanced urinary buffer capacity, an additional group (group 1B, N = 5) with NHP and chronic HCl acidosis was administered the non-Pi buffer, neutral creatinine (5.0 mmoles/kg daily). As with Pi, acidosis was ameliorated by creatinine administration and sigma delta NAE increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1984

Effect of colchicine and calcitonin on calcemic response to metabolic acidosis.

To examine the mechanism responsible for enhanced calcium mobilization from bone in metabolic acidosis, we evaluated the effect of colchicine and calcitonin, two blockers of cell-mediated bone resorption, on the calcemic response to acute metabolic acidosis in thyroparathyroidectomized rats. Metabolic acidosis lasting 16 hr and induced by the feeding of NH4Cl led to a significant rise in serum calcium of 1.2 to 1.9 mg/dl. The administration of colchicine or calcitonin led to a decrement in serum calcium of 1.1 +/- 0.2 (P less than 0.01) and 0.7 +/- 0.2 mg/dl (P less than 0.05), respectively. Cyclic AMP levels in calvaria from rats with metabolic acidosis and from control rats were not different. These data suggest that mobilization of calcium from bone which occurs in metabolic acidosis is due, in part, to increased bone resorption, which is mediated by a cAMP-independent mechanism.

Acidosis↗
PubMed1987

Acidosis, not azotemia, stimulates branched-chain, amino acid catabolism in uremic rats.

To investigate branched-chain, amino acid metabolism (BCAA) in muscle in chronic renal failure (CRF), we studied rats with moderately severe uremia (PUN 110 approximately mg/dl) and spontaneous metabolic acidosis (bicarbonate, 19 +/- 1 mEq/liter). Plasma BCAA levels in CRF compared to pair-fed control rats were approximately 15% lower and muscle valine was 93 microM lower (P less than 0.05). BCAA metabolism was measured in incubated epitrochlearis muscles using L-[1-14C]valine or L-[1-14C]leucine in the presence and absence of insulin. BCAA decarboxylation was increased (P less than 0.05) and insulin-stimulated BCAA incorporation into protein was blunted (P less than 0.05) by CRF. Since we have found that metabolic acidosis, by itself, stimulates muscle branched-chain, ketoacid dehydrogenase activity, another group of CRF and control rats was given NaHCO3 which corrected the acidosis, but not the azotemia. BCAA decarboxylation in muscle was reduced in CRF rats given NaHCO3, and this was reflected in increased plasma and muscle BCAA concentrations. We conclude that in CRF, chronic metabolic acidosis stimulates BCAA decarboxylation in skeletal muscle and this could contribute to the reduced intra- and extracellular concentrations of BCAA. Correction of acidosis should be a goal of therapy in CRF, especially when dietary regimens restrict intake of BCAA.

Acidosis↗
PubMed1993

Effect of metabolic acidosis on the expression of insulin-like growth factor and growth hormone receptor.

To further our understanding of the growth failure in metabolic acidosis, we examined the insulin-like growth factor (IGF-I and IGF-II), the IGF binding protein-3 (IGFBP-3), and the hepatic IGF mRNA and growth hormone receptor mRNA in control, pair-fed and acidotic rats. The rats in the last group were made acidotic by using ammonium chloride (1.5%) as their sole fluid intake for eight days. Metabolic acidosis was confirmed by a blood pH of 7.11 +/- 0.10 (mean +/- SD). The mean starting weights for all rats were 167.1 +/- 3.4 grams. Growth impairment was observed in the acidotic rats after one week of ammonium chloride intake. The body weights of the acidotic rats compared to those of the control rats were 155.5 +/- 18.9 g versus 222.8 +/- 9.7 g, P < 0.001; the pair-fed rats weighed 156.8 +/- 19.6 grams. All rats were bled and sacrificed on day 8. Sera and tissue were analyzed with the following results: compared to the ad libitum controls, the same IGF-I concentrations were significantly decreased in the acidotic animals (P < 0.02) as well as pair-fed controls (P < 0.005). The serum IGF-II and IGF-binding protein-3 concentrations were unchanged by acidosis or food restriction. The hepatic IGF-I mRNA was significantly reduced by acidosis (P < 0.01) and pair-feeding (P < 0.01). Compared to control, the mean hepatic IGF mRNA in acidosis was significantly lower (P < 0.01). However, there was no significant difference between the acidotic and the pair-fed groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1996

Correction of acidosis in CAPD decreases whole body protein degradation.

Correction of acidosis in CAPD decreases protein degradation and synthesis but has no effect on leucine oxidation. The effect of the correction of metabolic acidosis in CRF patients treated with CAPD was determined from the kinetics of infused L-[1-13C]leucine. Seven CAPD patients were studied before (acid) and after correction of acidosis (bicarbonate) (pH:acid 7.39 +/- 0.01, bicarbonate 7.41 +/- 0.01, P = 0.005). Leucine appearance from body protein (PD) [corrected] and leucine disappearance into body protein (PS) [corrected] decreased significantly with correction of acidosis. (PS: acid 211.7 +/- 9.8, bicarbonate 142.3 +/- 4.2 micromol x kg-1 x hr-1, P < 0.001; PD: acid 200.6 +/- 8.5, bicarbonate 132.4 +/- 3.7 micromol x kg-1 x hr-1, P < 0.001). There was no significant change in leucine oxidation or plasma amino acid concentrations. These results demonstrate that optimal correction of acidosis in CAPD is beneficial in terms of protein turnover.

Acidosis↗
PubMed1997

Regulation of AE1 anion exchanger and H(+)-ATPase in rat cortex by acute metabolic acidosis and alkalosis.

The cortical collecting duct (CCD) mediates net secretion or reabsorption of protons according to systemic acid/base status. Using indirect immunofluorescence, we examined the localization and abundance of the vacuolar H(+)-ATPase and the AE1 anion exchanger in intercalated cells (IC) of rat kidney connecting segment (CNT) and CCD during acute (6 hr) metabolic (NH4Cl) acidosis and respiratory (NaHCO3) alkalosis. AE1 immunostaining intensity quantified by confocal microscopy was elevated in metabolic acidosis and substantially reduced in metabolic alkalosis. AE1 immunostaining was restricted to Type A IC in all conditions, and the fraction of AE1+IC was unchanged in CNT and CCd. Metabolic acidosis was accompanied by redistribution of H(+)-ATPase immunostaining towards the apical surface of IC, and metabolic alkalosis was accompanied by H(+)-ATPase redistribution towards the basal surface of IC. Therefore, acute metabolic acidosis produced changes consistent with increased activity of Type A IC and decreased activity of Type B IC, whereas acute metabolic alkalosis produced changes corresponding to increased activity of Type B IC and decreased activity of Type A IC. These data demonstrate that acute systemic acidosis and alkalosis modulate the cellular distribution of two key transporters involved in proton secretion in the distal nephron.

Acid-Base Equilibrium↗
PubMed1986

The effect of metabolic acidosis on the synthesis and turnover of rat renal phosphate-dependent glutaminase.

Regulation of the mitochondrial phosphate-dependent glutaminase activity is an essential component in the control of renal ammoniagenesis. Alterations in acid-base balance significantly affect the amount of the glutaminase that is present in rat kidney, but not in brain or small intestine. The relative rates of glutaminase synthesis were determined by comparing the amount of [35S]methionine incorporated into specific immunoprecipitates with that incorporated into total protein. In a normal animal, the rate of glutaminase synthesis constitutes 0.04% of the total protein synthesis. After 7 days of metabolic acidosis, the renal glutaminase activity is increased to a value that is 5-fold greater than normal. During onset of acidosis, the relative rate of synthesis increases more rapidly than the appearance of increased glutaminase activity. The increased rate of synthesis reaches a plateau within 5 days at a value that is 5.3-fold greater than normal. Recovery from chronic acidosis causes a rapid decrease in the relative rate of glutaminase synthesis, but a gradual decrease in glutaminase activity. The former returns to normal within 2 days, whereas the latter requires 11 days. The apparent half-time for glutaminase degradation was found to be 5.1 days and 4.7 days for normal and acidotic rats respectively. These results indicate that the increase in renal glutaminase activity associated with metabolic acidosis is due primarily to an increase in its rate of synthesis. From the decrease in activity that occurs upon recovery from acidosis, the true half-life for the glutaminase was estimated to be 3 days.

Acidosis↗