scholarly journals INDUCED METABOLIC ACIDOSIS BY AMMONIUM CHLORIDE: ACTION MECHANISMS, DOSE AND EFFECTS ON ATHLETIC PERFORMANCE

2017 ◽  
Vol 28 (1) ◽  
Author(s):  
Carlos Rafaell Correia-Oliveira ◽  
Maria Augusta Peduti Dal’Molin Kiss
Keyword(s):  
Metabolic Acidosis ◽  
Ammonium Chloride ◽  
Athletic Performance ◽  
Action Mechanisms

Brain pH responses to sodium bicarbonate and Carbicarb during systemic acidosis

1989 ◽  
Vol 256 (5) ◽  
pp. H1316-H1321 ◽  
Author(s):  
J. I. Shapiro ◽  
M. Whalen ◽  
R. Kucera ◽  
N. Kindig ◽  
G. Filley ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Ammonium Chloride ◽  
Respiratory Acidosis ◽  
Arterial Pco2 ◽  
Bicarbonate Therapy ◽  
Brain Ph ◽  
Dose Dependent ◽  
Intracellular Alkalinization

Rats subjected to ammonium chloride-induced metabolic acidosis or respiratory acidosis caused by hypercapnia were given alkalinization therapy with either sodium bicarbonate or Carbicarb. Ammonium chloride induced dose-dependent systemic acidosis but did not affect intracellular brain pH. Hypercapnia caused dose-dependent systemic acidosis as well as decreases in intracellular brain pH. Sodium bicarbonate treatment resulted in systemic alkalinization and increases in arterial PCO2 in both acidosis models, but it caused intracellular brain acidification in rats with ammonium chloride acidosis. Carbicarb therapy resulted in systemic alkalinization without major changes in arterial PCO2 and intracellular brain alkalinization in both acidosis models. These data demonstrate that bicarbonate therapy of systemic acidosis may be associated with "paradoxical" intracellular brain acidosis, whereas Carbicarb causes both systemic and intracellular alkalinization under conditions of fixed ventilation.

Stimulation of an N-ethylmaleimide-sensitive ATPase in the collecting duct segments of the rat nephron by metabolic acidosis

1985 ◽  
Vol 63 (10) ◽  
pp. 1291-1296 ◽  
Author(s):  
Lal C. Garg ◽  
Neelam Narang
Keyword(s):  
Enzyme Activity ◽  
Plasma Membrane ◽  
Metabolic Acidosis ◽  
Ammonium Chloride ◽  
Atp Hydrolysis ◽  
Collecting Duct ◽  
Plasma Membrane Atpase ◽  
Membrane Atpase ◽  
Chloride Treatment ◽  
Stimulation Of

A plasma membrane ATPase sensitive to inhibition by N-ethylmaleimide (NEM) and insensitive to inhibition by oligomycin and ouabain has been shown to be involved in acidification of urine in the turtle bladder. The activity of this NEM-sensitive ATPase was determined in four types of distal nephron segments of normal rats and in rats treated with ammonium chloride. The enzyme activity was determined by a fluorometric micromethod in which ATP hydrolysis was coupled to NADH oxidation. Significant activities (10–35 pmol ADP∙min−1∙mm−1) of NEM-sensitive ATPase were present in the distal convoluted tubule (DCT) and in the cortical and outer and inner medullary collecting duet segments of normal rats. In metabolic acidosis produced by ammonium chloride treatment (plasma CO2 content = 15.3 ± 0.8 mequiv./L), the NEM-sensitive ATPase activity was increased significantly (60–100%) in the collecting duct segments without showing a significant change in the enzyme activity in the DCT. Our data are consistent with the hypothesis that a plasma membrane H+-ATPase (inhibited by NEM but not by oligomycin or ouabain) is involved in H+ secretion in the mammalian collecting duct.

Chronic acidosis-induced alteration in bone bicarbonate and phosphate

2003 ◽  
Vol 285 (3) ◽  
pp. F532-F539 ◽  
Author(s):  
David A. Bushinsky ◽  
Susan B. Smith ◽  
Konstantin L. Gavrilov ◽  
Leonid F. Gavrilov ◽  
Jianwei Li ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Ammonium Chloride ◽  
Acidic Medium ◽  
Urinary Calcium ◽  
Neonatal Mouse ◽  
Control Medium ◽  
Cross Sectional ◽  
Significant Fall

Chronic metabolic acidosis increases urinary calcium excretion without altering intestinal calcium absorption, suggesting that bone mineral is the source of the additional urinary calcium. In vivo and in vitro studies have shown that metabolic acidosis causes a loss of mineral calcium while buffering the additional hydrogen ions. Previously, we studied changes in femoral, midcortical ion concentrations after 7 days of in vivo metabolic acidosis induced by oral ammonium chloride. We found that, compared with mice drinking only distilled water, ammonium chloride induced a loss of bone sodium and potassium and a depletion of mineral HCO3− and phosphate. There is more phosphate than carbonate in neonatal mouse bone. In the present in vitro study, we utilized a high-resolution scanning ion microprobe with secondary ion mass spectroscopy to test the hypothesis that chronic acidosis would decrease bulk (cross-sectional) bone phosphate to a greater extent than HCO3− by localizing and comparing changes in bone HCO3− and phosphate after chronic incubation of neonatal mouse calvariae in acidic medium. Calvariae were cultured for a total of 51 h in medium acidified by a reduction in HCO3− concentration ([HCO3−]; pH ∼7.14, [HCO3−] ∼13) or in control medium (pH ∼7.45, HCO3− ∼26). Compared with incubation in control medium, incubation in acidic medium caused no change in surface total phosphate but a significant fall in cross-sectional phosphate, with respect to the carbon-carbon bond (C2) and the carbon-nitrogen bond (CN). Compared with incubation in control medium, incubation in acidic medium caused no change in surface HCO3− but a significant fall in cross-sectional HCO3− with respect to C2 and CN. The fall in cross-sectional phosphate was significantly greater than the fall in cross-sectional HCO3−. The fall in phosphate indicates release of mineral phosphates, and the fall in HCO3− indicates release of mineral HCO3−, both of which would be expected to buffer the additional protons and help restore the pH toward normal. Thus a model of chronic acidosis depletes bulk bone proton buffers, with phosphate depletion exceeding that of HCO3−.

scholarly journals Impaired urinary ammonium excretion in patients with isolated proximal renal tubular acidosis.

1993 ◽  
Vol 4 (4) ◽  
pp. 1073-1078 ◽  
Author(s):  
L G Brenes ◽  
M I Sanchez
Keyword(s):  
Metabolic Acidosis ◽  
Ammonium Chloride ◽  
Renal Tubular Acidosis ◽  
Ammonium Excretion ◽  
Loading Test ◽  
The Third ◽  
Titratable Acid ◽  
Proximal Renal Tubular Acidosis ◽  
Renal Tubular ◽  
Acid Loading

During previous studies in patients with isolated proximal renal tubular acidosis (pRTA), the rates of urinary ammonium excretion were considered inappropriately low for their state of chronic metabolic acidosis. These observations were made while the patients were on a normal diet as well as when they were undergoing a short ammonium chloride test. Because these findings suggested an impaired ability to excrete maximal amounts of ammonium, the response to the 3-day acid loading test was evaluated in eight patients with isolated pRTA and in 10 normal control subjects. Plasma creatinine, acid-base, and electrolyte values were analyzed before and after 3 days of ingesting 2 mmol/kg.24 h of ammonium chloride. Twenty-four-hour urine specimens were collected the day before and on the third day of acid loading to determine urine pH, as well as the rate of excretion of NH4+ and titratable acid in milliequivalents per 24 h per 1.73 m2. During the basal state, all patients with pRTA had hyperchloremic metabolic acidosis and they excreted urine of lower pH (5.51 +/- 0.18 versus 6.00 +/- 0.13; P < 0.05) and greater titratable acid (29.1 +/- 4.3 versus 21.8 +/- 1.4; P < 0.05); however, they had rates of NH4+ excretion similar to those of controls. On the third day of acid loading, they excreted urine of lower pH (4.66 +/- 0.03 versus 5.00 +/- 0.03; P < 0.05) and equivalent amounts of titratable acid, whereas their NH4+ excretion was significantly less than that of controls (47.7 +/- 4.4 versus 76.3 +/- 5.7; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Severe uncompensated metabolic acidosis secondary to ammonium chloride loading

1977 ◽  
Vol 91 (2) ◽  
pp. 263-265 ◽  
Author(s):  
Francis J. DiBona ◽  
Robert C. Kelsch
Keyword(s):  
Metabolic Acidosis ◽  
Ammonium Chloride

Effect of NH4Cl on phosphaturic response to PTH in the hamster: dissociation from acidemia

1980 ◽  
Vol 239 (5) ◽  
pp. E328-E332
Author(s):  
A. Hoppe ◽  
M. Destro ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Ammonium Chloride ◽  
Respiratory Acidosis ◽  
Fractional Excretion ◽  
Ammonium Bicarbonate ◽  
Ammonium Ion ◽  
Fractional Excretion Of Phosphate

Previous studies indicate that the hamster fasted for 16 h fails to demonstrate a significant phosphaturic response to parathyroid hormone (PTH). However, when hamsters were infused with ammonium chloride, a phosphaturic response to PTH was observed. The present studies evaluate the respective roles of acidemia and the ammonium ion in this response. As in previous studies, fasted thyroparathyroidectomized (TPTX) hamsters infused with PTH showed no significant increase in the fractional excretion of phosphate (FE rho), from 19 +/- 2 to 22 +/- 1%. Neither respiratory acidosis (hypercapnia) nor metabolic acidosis (HCl infusion) enhanced the phosphaturic effect of PTH, FE rho 21 +/- 4 to 20 +/- 6 and 15 +/- 2 to 16 +/- 3%, respectively. Both ammonium chloride and ammonium bicarbonate infusions enhanced the phosphaturic response; FE rho increased from 15 +/- 5 to 27 +/- 5% (P < 0.02) and 17 +/- 3 to 25 +/- 3% (P < 0.05), respectively. We conclude that the enhancement of the phosphaturic effect of PTH in the fasted hamster by ammonium chloride infusions can be dissociated from acidemia.

Chronic metabolic acidosis augments acidification along the inner medullary collecting duct

1986 ◽  
Vol 250 (4) ◽  
pp. F690-F694 ◽  
Author(s):  
H. H. Bengele ◽  
J. H. Schwartz ◽  
E. R. McNamara ◽  
E. A. Alexander
Keyword(s):  
Metabolic Acidosis ◽  
Acid Secretion ◽  
Ammonium Chloride ◽  
Collecting Duct ◽  
Major Site ◽  
Chronic Metabolic Acidosis ◽  
Inner Medullary Collecting Duct ◽  
Titratable Acid ◽  
Arterial Ph ◽  
Medullary Collecting Duct

The inner medullary collecting duct (IMCD) of the rat is a major site of acidification. However, previous micropuncture studies have failed to demonstrate acidification along the terminal IMCD during chronic acid feeding. To more completely evaluate this question we used the microcatheterization method in rats fed ammonium chloride for 3-7 days. Arterial pH was 7.30 +/- 0.015, and PCO2 was set at 40 +/- 0.6 mmHg. The IMCD data were analyzed as a function of IMCD length between 40% and the tip. Equilibrium pH decreased from 6.21 +/- 0.11 to 5.47 +/- 0.03, whereas PCO2 was unchanged (28 +/- 1 mmHg between the deep samples and tip). Bicarbonate delivery decreased from 92 +/- 14 to 10 +/- 1 nmol/min, titratable acid increased from 462 +/- 33 to 762 +/- 40 nmol/min, and ammonium delivery increased from 2,235 +/- 121 to 3,528 +/- 140 nmol/min. Thus estimated net acid increased from 2,638 +/- 134 to 4,303 +/- 161 nmol/min. To determine whether increasing delivery of buffer to the IMCD would stimulate acid secretion in acute acidosis, rats were studied during the infusion of HCl and creatinine. Arterial pH was 7.18 +/- 0.02. IMCD acidification was not increased compared with our previously published studies during HCl infusion [Am. J. Physiol. 241 (Renal Fluid Electrolyte Physiol. 10): F669-F676, 1981]. We conclude that chronic ammonium chloride ingestion stimulates IMCD acidification and that this increase may be an intrinsic modification of the acidification mechanism of the IMCD.

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