Acute and Chronic Metabolic Acidosis in the Pig: Renal Metabolism and Ammoniagenesis1

2015 ◽  
pp. 18-30 ◽  
Author(s):  
E. Junco ◽  
R. Perez ◽  
R. Jofre ◽  
S. Alonso ◽  
A. Martinez ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Renal Metabolism ◽  
Chronic Metabolic Acidosis

Inhibition of 25-hydroxyvitamin D3-1-hydroxylase by chronic metabolic acidosis

1982 ◽  
Vol 243 (4) ◽  
pp. E265-E271
Author(s):  
G. S. Reddy ◽  
G. Jones ◽  
S. W. Kooh ◽  
D. Fraser
Keyword(s):  
Vitamin D ◽  
Metabolic Acidosis ◽  
Rat Kidney ◽  
Ion Concentration ◽  
Hydroxylase Activity ◽  
Renal Metabolism ◽  
Dihydroxyvitamin D3 ◽  
Hydrogen Ion Concentration ◽  
Chronic Metabolic Acidosis ◽  
Negative Linear Correlation

Chronic metabolic acidosis had been shown to influence the renal metabolism of 25-hydroxyvitamin D3. Using the isolated perfused rat kidney model, we evaluated the rates of synthesis of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] in vitamin D-depleted [D(-)] and 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] in vitamin D-replete [D(+)] rats. Metabolic acidosis was induced in both groups of rats by feeding aqueous ammonium chloride for 9 days. Kidneys isolated from D(-) acidotic rats (mean pH, 7.11) exhibited a decreased rate of 1,25(OH)2D3 synthesis (0.79 +/- 0.17 pmol produce . h-1 . g kidney-1) when compared with that (1.27 +/- 0.09) of D(-) nonacidotic (mean pH, 7.33) rats. There was a significant negative linear correlation between the rate of synthesis of 1,25(OH)2D3 and the hydrogen ion concentration of the animal (r = 0.79, P less than 0.005). The rate of synthesis of 24,25(OH)2D3 by the kidneys from D(+) acidotic (mean pH, 7.06) and nonacidotic (mean pH, 7.39) rats did not differ (0.81 +/- 0.21 vs. 0.60 +/- 0.12 pmol product . h-1 . g kidney-1). It is concluded that chronic acidosis suppressed 1-hydroxylase activity, but does not suppress 24-hydroxylase activity.

scholarly journals Remnant kidney metabolism in the dog.

1991 ◽  
Vol 2 (1) ◽  
pp. 70-76
Author(s):  
A Fine
Keyword(s):  
Glomerular Filtration Rate ◽  
Metabolic Acidosis ◽  
Oxygen Uptake ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Normal Kidney ◽  
Renal Metabolism ◽  
Energy Substrates ◽  
Chronic Metabolic Acidosis ◽  
Remnant Kidney

A marked increase in oxygen uptake (Qo2) per nephron has been described in the remnant kidney of the rat. However, it is not known which substrates support renal metabolism in remnant kidney nor is it known whether similar changes in Qo2 occur in other species. Remnant kidney in the dog was induced by ligation of 60 to 75% of the renal arterial branches on one side followed 1 to 2 wk later by contralateral nephrectomy. At 3 months marked hypertrophy of the remnant kidney was found and the glomerular filtration rate was 18 +/- 1.8 mL/min compared with 31 +/- 2 in a normal kidney (P less than 0.01). Qo2 was 689 +/- 60 mumol/min/100 mL glomerular filtration rate in the remnant kidney compared with 564 +/- 42 mumol/min/100 mL glomerular filtration rate in the normal kidney (P less than 0.01). Total renal ammoniagenesis per nephron increased to values found in chronic metabolic acidosis although serum (K+) and (HCO3-) were no different than in the normal dog. The oxidation of glutamine and lactate by remnant kidneys accounted for over 80% of Qo2, similar to that of normal kidneys. It is concluded that hypermetabolism per nephron occurs in the remnant kidney of the dog and that glutamine and lactate are the major energy substrates in remnant kidney. Furthermore, factors other than serum (K+) and (HCO3-) augment ammoniagenesis in this model. However, when these results are expressed per whole kidney or per gram of tissue, hypermetabolism does not occur in these remnant kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Expression of rat thick limb Na/H exchangers in potassium depletion and chronic metabolic acidosis

2001 ◽  
Vol 60 (4) ◽  
pp. 1386-1396 ◽  
Author(s):  
Kamel Laghmani ◽  
Christine Richer ◽  
Pascale Borensztein ◽  
Michel Paillard ◽  
Marc Froissart
Keyword(s):  
Metabolic Acidosis ◽  
Potassium Depletion ◽  
Chronic Metabolic Acidosis

The Effect of Chronic Metabolic Acidosis on the End Organ Responsiveness to Parathyroid Hormone in Man*

1983 ◽  
Vol 56 (3) ◽  
pp. 619-622 ◽  
Author(s):  
JEFFREY A KRAUT ◽  
EARL M. GORDON ◽  
JOHN C. RANSOM ◽  
JACK W. COBURN ◽  
KIYOSHI KUROKAWA
Keyword(s):  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Chronic Metabolic Acidosis

Basolateral membrane H-OH-HCO3 transport in the proximal tubule

1989 ◽  
Vol 256 (5) ◽  
pp. F751-F765
Author(s):  
P. A. Preisig ◽  
R. J. Alpern
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Basolateral Membrane ◽  
Respiratory Acidosis ◽  
Cell Voltage ◽  
Transport Mechanisms ◽  
Transport Capacity ◽  
Chronic Metabolic Acidosis

This review focuses on the basolateral membrane mechanisms of H-OH-HCO3 transport in the proximal tubule. The mechanism that has the greatest transport capacity and mediates most of transepithelial H-HCO3 transport is the electrogenic, Na-3HCO3 cotransporter. This transporter has been extensively characterized in the salamander, rat, and rabbit proximal tubule, and has now been found in a number of other epithelia that effect transepithelial NaHCO3 transport. Transporter rate is sensitive to intra- and extracellular [Na], intra- and extracellular [HCO3]/pH, and cell voltage. Adaptations in transporter activity have been demonstrated in chronic metabolic acidosis and alkalosis, chronic respiratory acidosis and alkalosis, and chronic hyperfiltration. In addition to the Na-3HCO3 cotransporter, the basolateral membrane possesses both Na-dependent and -independent Cl-HCO3 exchangers, a H leak, and in the S3 proximal tubule an Na-H antiporter. The role of these H-OH-HCO3 transport mechanisms in transcellular HCO3 and Cl absorption and pHi defense is discussed.

Effect of chronic metabolic acidosis on net electrolyte transport in rat colon

1989 ◽  
Vol 256 (6) ◽  
pp. G1036-G1040 ◽  
Author(s):  
G. M. Feldman
Keyword(s):  
Metabolic Acidosis ◽  
Distal Colon ◽  
Distal Segment ◽  
Proximal Colon ◽  
Electrolyte Transport ◽  
Rat Colon ◽  
Chronic Metabolic Acidosis ◽  
In Situ Perfusion ◽  
Arterial Blood ◽  
Acute Correction

Rats fed NH4Cl (5 meq.100 g body wt-1.day-1) for one week developed chronic metabolic acidosis and had an arterial blood pH and plasma HCO3- concentration of 7.27 +2- 0.02 and 16.2 +/- 0.8 meq/l, respectively; control animals had values of 7.36 +/- 0.01 and 22.4 +/- 0.5 meq/l, respectively. Net electrolyte transport was measured in proximal and distal colonic segments by in situ perfusion. In proximal colon, chronic metabolic acidosis increased HCO3- absorption from 3.3 +/- 0.8 to 6.4 +/- 0.6 mu eq.min-1.g-1 but did not alter Na+ absorption. In distal colon, although Na+ transport was unaffected, chronic acidosis reduced HCO3- secretion from -6.9 +/- 0.8 to -4.4 +/- 0.7 mu eq.min-1.g-1 and increased voltage from -18.9 +/- 2.0 to -51.1 +/- 4.2 mV. To evaluate the dependence of these effects on altered arterial pH and HCO3- concentration, NaHCO3 was infused intravenously, raising pH and HCO3- concentration to 7.53 +/- 0.04 and 23.9 +/- 1.7 meq/l, respectively. Although acute correction of chronic metabolic acidosis reduced HCO3- absorption in proximal colon, it did not affect HCO3- secretion or voltage in the distal segment, suggesting that proximal and distal colon respond differently to chronic metabolic acidosis. These results also suggest that chronic metabolic acidosis alters the mechanisms of ion transport in distal colon.

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

Evaluation of urine acidification by urine anion gap and urine osmolal gap in chronic metabolic acidosis

1996 ◽  
Vol 27 (1) ◽  
pp. 42-47 ◽  
Author(s):  
Gheun-Ho Kim ◽  
Jin Suk Han ◽  
Yon Su Kim ◽  
Kwon Wook Joo ◽  
Suhnggwon Kim ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Anion Gap ◽  
Chronic Metabolic Acidosis ◽  
Urine Acidification ◽  
Osmolal Gap
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