Effects of L-Glutamate Infusion on the Renal Utilization of Glutamate and Glutamine in the Dog Kidney in vivo during Chronic Metabolic Acidosis or Alkalosis

2015 ◽  
pp. 114-124 ◽  
Author(s):  
G. Frindt ◽  
J. Lizana ◽  
G. Diaz ◽  
G. Gonzalez ◽  
E. Bourke
Keyword(s):  
Metabolic Acidosis ◽  
Chronic Metabolic Acidosis ◽  
Dog Kidney

scholarly journals The kidney of chicken adapts to chronic metabolic acidosis: In vivo and in vitro studies

1982 ◽  
Vol 22 (2) ◽  
pp. 103-111 ◽  
Author(s):  
André G. Craan ◽  
◽  
Guy Lemieux ◽  
Patrick Vinay ◽  
André Gougoux
Keyword(s):  
Metabolic Acidosis ◽  
In Vitro Studies ◽  
Chronic Metabolic Acidosis

scholarly journals Glucose Utilization and Production by the Dog Kidney In Vivo in Metabolic Acidosis and Alkalosis

1973 ◽  
Vol 52 (3) ◽  
pp. 608-611 ◽  
Author(s):  
J. Costello ◽  
J. M. Scott ◽  
P. Wilson ◽  
E. Bourke
Keyword(s):  
Metabolic Acidosis ◽  
Glucose Utilization ◽  
Dog Kidney

Intracellular bicarbonate of skeletal muscle under different metabolic states

1976 ◽  
Vol 230 (1) ◽  
pp. 228-232 ◽  
Author(s):  
RN Khuri ◽  
SK Agulian ◽  
KK Bogharian
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Metabolic Alkalosis ◽  
Equilibrium Potential ◽  
Chronic Metabolic Acidosis ◽  
Cell Ph ◽  
Metabolic States ◽  
Na Depletion ◽  
K Depletion

Intracellular bicarbonate of single muscle fibers in vivo was measured by a direct electrometric method simultaneously with the membrane PD in rats under seven different metabolic states. From the measured intracellular bicarbonate values and the PCO2, the bicarbonate equilibrium potential and the intracellular pH were calculated. The mean intracellular [HCO3-] under normal control conditions was 10.3 +/- 0.7 mM (SE). The intracellular bicarbonate fell significantly in both chronic metabolic acidosis and chronic K+ depletion. In contrast, intracellular bicarbonate was elevated in chronic metabolic alkalosis, K+ loading, and Na+ depletion. Taking intracellular pH as an index of the acid-base status of cells, we find that whereas the calculated cell pH decreased along with the cell bicarbonate in both chronic metabolic acidosis and K+ depletion, cell pH increased along with the bicarbonate only in chronic metabolic alkalosis. Cell pH was unchanged in both chronic K+ loading and Na+ depletion.

31P-NMR in vivo measurement of renal intracellular pH: effects of acidosis and K+ depletion in rats

1986 ◽  
Vol 251 (5) ◽  
pp. F904-F910 ◽  
Author(s):  
W. R. Adam ◽  
A. P. Koretsky ◽  
M. W. Weiner
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Respiratory Acidosis ◽  
Resonance Spectroscopy ◽  
Ph Effects ◽  
Potassium Depletion ◽  
Chronic Metabolic Acidosis ◽  
Arterial Blood ◽  
Blood Ph

Renal intracellular pH (pHi) was measured in vivo from the chemical shift (sigma) of inorganic phosphate (Pi), obtained by 31P-nuclear magnetic resonance spectroscopy (NMR). pH was calculated from the difference between sigma Pi and sigma alpha-ATP. Changes of sigma Pi closely correlated with changes of sigma monophosphoesters; this supports the hypothesis that the pH determined from sigma Pi represents pHi. Renal pH in control rats was 7.39 +/- 0.04 (n = 8). This is higher than pHi of muscle and brain in vivo, suggesting that renal Na-H antiporter activity raises renal pHi. To examine the relationship between renal pH and ammoniagenesis, rats were subjected to acute (less than 24 h) and chronic (4-7 days) metabolic acidosis, acute (20 min) and chronic (6-8 days) respiratory acidosis, and dietary potassium depletion (7-21 days). Acute metabolic and respiratory acidosis produced acidification of renal pHi. Chronic metabolic acidosis (arterial blood pH, 7.26 +/- 0.02) lowered renal pHi to 7.30 +/- 0.02, but chronic respiratory acidosis (arterial blood pH, 7.30 +/- 0.05) was not associated with renal acidosis (pH, 7.40 +/- 0.04). At a similar level of blood pH, pHi was higher in chronic metabolic acidosis than in acute metabolic acidosis, suggesting an adaptive process that raises pHi. Potassium depletion (arterial blood pH, 7.44 +/- 0.05) was associated with a marked renal acidosis (renal pH, 7.17 +/- 0.02). There was a direct relationship between renal pH and cardiac K+. Rapid partial repletion with KCl (1 mmol) significantly increased renal pHi from 7.14 +/- 0.03 to 7.31 +/- 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

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

1982 ◽  
Vol 60 (12) ◽  
pp. 1431-1435 ◽  
Author(s):  
Mitchell L. Halperin ◽  
Robert L. Jungas ◽  
Carole Pichette ◽  
Marc B. Goldstein
Keyword(s):  
Metabolic Acidosis ◽  
Quantitative Analysis ◽  
Maximum Rate ◽  
Intact Animal ◽  
Maximum Velocity ◽  
Chronic Metabolic Acidosis ◽  
Atp Production ◽  
Ammonium Production ◽  
Substrate Concentrations

Many theories have been proposed to explain the regulation of renal ammoniagenesis during chronic metabolic acidosis but none of these is entirely satisfactory. Since the activity of each of the enzymes in this pathway greatly exceeds the maximum rate of ammonium production in vivo, even when physiological substrate concentrations are used in this calculation, it follows that ammoniagenesis must be inhibited in the intact animal. We shall present a novel hypothesis for the regulation of the maximum rate of ammoniagenesis which emphasizes the fact that ATP is a product of this pathway and that a limited rate of ATP utilization could control its maximum velocity during chronic metabolic acidosis. To test the validity of our hypothesis, a quantitative analysis of the pathways of ATP production and utilization in the kidney will be reviewed. This approach is similar to one already proposed for the regulation of the maximum rate of ketogenesis in the liver.

Effect of chronic metabolic acidosis on bone density and bone architecture in vivo in rats

2014 ◽  
Vol 306 (5) ◽  
pp. F517-F524 ◽  
Author(s):  
Jürg A. Gasser ◽  
Henry N. Hulter ◽  
Peter Imboden ◽  
Reto Krapf
Keyword(s):  
Metabolic Acidosis ◽  
Bone Resorption ◽  
Bone Mass ◽  
Cortical Bone ◽  
Bone Microarchitecture ◽  
Chronic Metabolic Acidosis ◽  
Ovx Rats ◽  
Cortical Bone Mass ◽  
Trabecular Number

Chronic metabolic acidosis (CMA) might result in a decrease in vivo in bone mass based on its reported in vitro inhibition of bone mineralization, bone formation, or stimulation of bone resorption, but such data, in the absence of other disorders, have not been reported. CMA also results in negative nitrogen balance, which might decrease skeletal muscle mass. This study analyzed the net in vivo effects of CMA's cellular and physicochemical processes on bone turnover, trabecular and cortical bone density, and bone microarchitecture using both peripheral quantitative computed tomography and μCT. CMA induced by NH4Cl administration (15 mEq/kg body wt/day) in intact and ovariectomized (OVX) rats resulted in stable CMA (mean Δ[HCO3−]p = 10 mmol/l). CMA decreased plasma osteocalcin and increased TRAP5b in intact and OVX animals. CMA decreased total volumetric bone mineral density (vBMD) after 6 and 10 wk ( week 10: intact normal +2.1 ± 0.9% vs. intact acidosis −3.6 ± 1.2%, P < 0.001), an effect attributable to a decrease in cortical thickness and, thus, cortical bone mass (no significant effect on cancellous vBMD, week 10) attributed to an increase in endosteal bone resorption (nominally increased endosteal circumference). Trabecular bone volume (BV/TV) decreased significantly in both CMA groups at 6 and 10 wk, associated with a decrease in trabecular number. CMA significantly decreased muscle cross-sectional area in the proximal hindlimb at 6 and 10 wk. In conclusion, chronic metabolic acidosis induces a large decrease in cortical bone mass (a prime determinant of bone fragility) in intact and OVX rats and impairs bone microarchitecture characterized by a decrease in trabecular number.

Determinants of ammonia entry along the rat proximal tubule during chronic metabolic acidosis

1989 ◽  
Vol 256 (6) ◽  
pp. F1104-F1110 ◽  
Author(s):  
E. E. Simon ◽  
C. Merli ◽  
J. Herndon ◽  
E. J. Cragoe ◽  
L. L. Hamm
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Flow Rate ◽  
Significant Inhibition ◽  
Perfusion Rate ◽  
Chronic Metabolic Acidosis ◽  
Bicarbonate Reabsorption ◽  
Rate Dependent ◽  
Rat Proximal Tubule

The technique of in vivo microperfusion was used to examine the determinants of ammonia entry along the rat proximal tubule under conditions of chronic metabolic acidosis (CMA). When perfused with a 5 mM bicarbonate-containing perfusate, collected fluid ammonia concentrations remained constant with increasing flow rate and thus ammonia entry was highly flow-rate dependent. Ammonia entry was also flow-rate dependent using a 25 mM bicarbonate perfusate but entry reached a plateau as perfusion rate increased. Also, ammonia entry tended to be lower at all perfusion rates with the 25 mM perfusate compared with the 5 mM bicarbonate perfusate, but this was most evident at the highest perfusion rate (45 nl/min). The decline in ammonia entry was associated with increasing collected fluid bicarbonate concentrations, suggesting that there was inhibition of diffusion trapping of ammonia. The effects of Na+-H+ exchange inhibition on ammonia entry were examined using the amiloride analogue, 5-(N-ethyl-N-isopropyl)amiloride. With a 25 mM bicarbonate-containing perfusate, the amiloride analogue caused a significant decrease in bicarbonate reabsorption but a nonsignificant decrease in ammonia entry associated with a significant rise in collected fluid bicarbonate concentration. When the potential effects of decreased diffusion trapping of ammonia were eliminated with 12 and 5 mM bicarbonate-containing perfusates, the analogue had no effect on ammonia entry despite significant inhibition of bicarbonate reabsorption. Thus ammonia entry in CMA is moderately affected by tubule fluid pH but is highly flow-rate dependent. There were no effects of inhibition of Na+-H+ exchange above those expected from inhibition of diffusion trapping of ammonia.

Immediate adaptation of the dog kidney to acute hypercapnia

1982 ◽  
Vol 243 (3) ◽  
pp. F227-F234
Author(s):  
A. Gougoux ◽  
P. Vinay ◽  
M. Cardoso ◽  
M. Duplain ◽  
G. Lemieux
Keyword(s):  
Blood Flow ◽  
Metabolic Acidosis ◽  
Renal Blood Flow ◽  
Respiratory Acidosis ◽  
Metabolite Profile ◽  
Ammonia Production ◽  
Glutamine Concentration ◽  
Hemodynamic Changes ◽  
Chronic Metabolic Acidosis ◽  
Dog Kidney

Studies were performed to determine whether ammoniagenesis could adapt instantaneously to acidosis in the dog kidney. Following acute respiratory acidosis, renal glutamine extraction rose acutely in dogs with stable renal blood flow but did not change when the renal blood flow fell by more than 25%. Acute hypercapnia immediately increased renal ammonia production in both groups of dogs. The rate of both glutamine extraction and ammonia production in acutely hypercapnic dogs without hemodynamic changes was comparable to the rates observed in dogs with chronic metabolic acidosis. Furthermore, the renal metabolite profile observed in acute hypercapnia was similar to the pattern described in chronic metabolic acidosis, i.e., a marked fall in renal glutamate and alpha-ketoglutarate concentrations and a fivefold increase in malate and oxaloacetate concentrations. In the liver and muscle, acute hypercapnia induced no significant change in glutamine concentration but glutamate and alpha-ketoglutarate concentrations decreased. Our findings demonstrate that the dog kidney can adapt immediately to acidosis but that hemodynamic change may mask this adaptation.

Substrate utilization by the distal nephron in dogs with chronic metabolic acidosis: studies with ethacrynic acid

1985 ◽  
Vol 63 (12) ◽  
pp. 1565-1569 ◽  
Author(s):  
Mitchell L. Halperin ◽  
Ching B. Chen
Keyword(s):  
Metabolic Acidosis ◽  
Ethacrynic Acid ◽  
Proximal Convoluted Tubule ◽  
Sodium Reabsorption ◽  
Thick Ascending Limb ◽  
Distal Nephron ◽  
Chronic Metabolic Acidosis ◽  
Fractional Excretion Of Sodium ◽  
Renal Oxygen Consumption ◽  
Dog Kidney

Glutamine and lactate oxidations provide the bulk of ATP required for sodium reabsorption in the dog kidney during chronic metabolic acidosis. Indirect evidence has suggested that glutamine is oxidized in the proximal convoluted tubule; if this is true, lactate should be the major fuel of the more distal nephron sites. The purpose of these experiments was to determine which substrates were metabolized by the acidotic dog kidney when a significant proportion of sodium chloride reabsorption was inhibited in the thick ascending limb of the loop of Henle. Ethacrynic acid, a loop diuretic, caused the fractional excretion of sodium to increase from 1 to 34%. The glomerular filtration rate declined somewhat, but there was no significant change in the renal blood flow rate. Renal oxygen consumption declined in conjunction with the natriuresis. However, when the data were examined at a constant filtered load of sodium (a constant rate of ATP turnover), there was no reduction in glutamine uptake or glutamine conversion to ATP in the presence of this natriuretic agent. The major change observed concerned lactate metabolism, in the presence of ethacrynic acid, there was no longer a significant rate of lactate extraction. These data are best explained by assuming that glutamine is the fuel of the proximal convoluted tubule of the acidotic dog kidney, whereas lactate oxidation occurs principally in the nephron sites where sodium reabsorption was inhibited by ethacrynic acid.

scholarly journals In vivo unaltered muscle protein synthesis in experimental chronic metabolic acidosis

1994 ◽  
Vol 46 (6) ◽  
pp. 1705-1712 ◽  
Author(s):  
Saâd Maniar ◽  
Denise Laouari ◽  
Michèle Dechaux ◽  
Véronique Motel ◽  
Jean-Pierre Yvert ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Metabolic Acidosis ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Chronic Metabolic Acidosis
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