scholarly journals Energy turnover and the production of ammonium by the kidney: effect of hypernatremia

1992 ◽  
Vol 70 (1) ◽  
pp. 8-12
Author(s):  
Mitchell L. Halperin ◽  
Ching-Bun Chen
Keyword(s):  
Body Weight ◽  
Oxygen Consumption ◽  
Metabolic Acidosis ◽  
Metabolic Regulation ◽  
Urine Flow ◽  
Acid Excretion ◽  
Acid Base ◽  
Energy Turnover ◽  
Chronic Metabolic Acidosis ◽  
Rate Of Oxygen Consumption

The purpose of this study was to explore further the relation between the rates of oxygen consumption and ammonium (NH4+) production in the kidney during chronic metabolic acidosis. The experimental model was the dog with chronic metabolic acidosis because of the extensive background literature in this species. Chronic metabolic acidosis was produced by the ingestion of 10 mmol NH4Cl/kg body weight for 5 days. There was a significant increase in the rate of oxygen extraction when hypernatremia was present. Despite this rise in the rate of oxygen consumption, there was no increase in the rate of NH4+ production nor in the rate of glutamine extraction. These data suggest that hypernatremia might prevent a further augmentation in glutamine extraction when the rate of oxygen consumption rises. In addition, a larger proportion of the NH4+ produced was excreted in the urine during hypernatremia. This increase was associated with a rise in the urine flow rate, but not with a fall in urine pH.Key words: Acid–base, ATP, glutamine, energy metabolism, metabolic acidosis, metabolic regulation, net acid excretion, oxygen consumption.

Influence of acute hyponatremia on renal ammoniagenesis in dogs with chronic metabolic acidosis

1990 ◽  
Vol 258 (2) ◽  
pp. F328-F332
Author(s):  
M. L. Halperin ◽  
B. C. Ching
Keyword(s):  
Oxygen Consumption ◽  
Metabolic Acidosis ◽  
Chronic Metabolic Acidosis ◽  
Rate Of Oxygen Consumption ◽  
Ammonium Production ◽  
Significant Change ◽  
Acute Hyponatremia ◽  
Rate Of Extraction

The purpose of this study was to determine how acute hyponatremia might augment the excretion of ammonium in dogs with chronic metabolic acidosis. The excretion of ammonium was higher during hyponatremia because the proportion of ammonium produced that was excreted in the urine increased from 66% in controls to 77%. Effects on the production of ammonium are more complex. The rate of renal ammoniagenesis was not increased during hyponatremia in absolute terms nor when expressed per millimole of oxygen consumption. In contrast, this rate was somewhat higher during hyponatremia if expressed per millimole of sodium reabsorbed (9.8 vs. 10.3 mumol). The rate of oxygen consumption by the kidney did not fall, as anticipated, during hyponatremia; when this rate was expressed per millimole of sodium reabsorbed it rose from 46 to 55 mumol. There was no significant change in the rate of extraction of glutamine by the kidney, but there was a significant decrease in the rate of release of alanine during hyponatremia. Hence there appears to be more oxidation (yielding more ammonium) and less transamination of glutamine. We conclude that the renal events which led to a higher rate of excretion of ammonium during hyponatremia were a larger than expected rate of ammonium production owing to a greater rate of oxygen consumption together with lesser rate of transamination of the glutamine extracted by the kidney. In addition, more of the ammonium produced was transferred to the urine.

Impact of hydrogen ion on fasting ketogenesis: feedback regulation of acid production

1982 ◽  
Vol 242 (3) ◽  
pp. F238-F245 ◽  
Author(s):  
V. L. Hood ◽  
E. Danforth ◽  
E. S. Horton ◽  
R. L. Tannen
Keyword(s):  
Acid Production ◽  
Metabolic Regulation ◽  
Feedback Regulation ◽  
Hydrogen Ion ◽  
Acid Excretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Urine Ph ◽  
Ion Production ◽  
Base Balance

To determine whether acid-base balance regulates hydrogen ion production, seven obese volunteers were given NaHCO3 and NH4Cl (2 mmol.kg-1.day-1) during two separate 7-day fasts. On days 5-7 plasma bicarbonate was lower in the NH4Cl fasts (14.0 +/- 1.4 mM) than in the NaHCO3 fasts (18.3 +/- 1.1 mM), while urine pH and net acid excretion did not differ. Acid production (acid excretion minus intake) was greater by 204 mmol/day in the NaHCO3 fasts (274 +/- 16 mmol/day) than in the NH4Cl fasts (70 +/- 19 mmol/day). Ketoacid excretion, which reflected net ketoacid production, paralleled acid production, decreasing from 213 +/- 24 mmol/day in the NaHCO3 fasts to 67 +/- 18 mmol/day in the NH4Cl fasts. Thus, during starvation, alterations in hydrogen ion intake and the associated changes in acid-base balance modify the net production of endogenous acid by influencing the synthesis or utilization of ketoacids. Although the specific site of this metabolic regulation is undefined, these results indicate that systemic acid-base status can exert feedback control over hydrogen ion production.

METABOLIC REFERENCE STANDARDS FOR THE NEONATE

PEDIATRICS ◽  
1967 ◽  
Vol 39 (5) ◽  
pp. 724-732
Author(s):  
John C. Sinclair ◽  
Jon W. Scopes ◽  
William A. Silverman
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Oxygen Consumption ◽  
Metabolic Rate ◽  
Extracellular Fluid ◽  
Mean Value ◽  
Reference Standards ◽  
Contributory Factor ◽  
Tissue Mass ◽  
Rate Of Oxygen Consumption

Oxygen consumption of 92 normally grown newborn babies of birth weight 750 to 3,940 gm has been expressed in terms of various metabolic reference standards in order to identify any systematic variation in expression of metabolic rate that is introduced by these bases of reference in the newborn population. It is postulated that differences in body composition comprise a contributory factor to the variation among newborn babies in rate of oxygen consumption per kilogram body weight. The predictive error from a mean value is increased if surface area, body weight, or fat-free body weight is substituted for body weight as a metabolic reference standard. By taking into account known changes in body composition of the fetus with increasing maturity, a compartment representing the active tissue mass is calculated. This corresponds closely to body weight minus extracellular fluid and includes fat. Rate of oxygen consumption is proportional to the size of this compartment over the range of body weights studied. Implications are discussed as to the metabolic rate of adipose tissue in the newborn and body composition among undergrown babies.

The relationship between cirral activity and oxygen uptake in Balanus balanoides

1965 ◽  
Vol 45 (2) ◽  
pp. 387-403 ◽  
Author(s):  
R. C. Newell ◽  
H. R. Northcroft
Keyword(s):  
Body Weight ◽  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
Mantle Cavity ◽  
The Body ◽  
Effect Of Temperature ◽  
Zero Rate ◽  
Rate Of Oxygen Consumption ◽  
The Relationship ◽  
Balanus Balanoides

The rate of cirral beat of Balanus balanoides is related to the logarithm of the body weight as an exponential function. In any one animal, there is little effect of temperature on cirral activity between 7·5° and 10° C. Between 10° and 20° C, however, there is a rapid increase in cirral beat with temperature followed by a fall at temperatures above 20° C.Balanus balanoides exhibits a fast, medium and zero rate of oxygen consumption. These rates of oxygen consumption correspond with (a) normal cirral beating, (b) ‘testing’ activity with no cirral movement, and (c) with the closure of the mantle cavity. Both of the possible levels of oxygen uptake are related to the logarithm of the body weight in a logarithmic fashion over the temperature range 7·5°–22·5° C. Temperature affects the two rates of oxygen consumption differently. In the slower rate (rate B) there is an increase in the rate of oxygen consumption between 7·5° and 14° C but there is no significant increase in the rate of oxygen consumption between 14° and 22·5 C°.

Chronic metabolic acidosis upregulates rat kidney Na-HCO 3 − cotransporters NBCn1 and NBC3 but not NBC1

2002 ◽  
Vol 282 (2) ◽  
pp. F341-F351 ◽  
Author(s):  
Tae-Hwan Kwon ◽  
Christiaan Fulton ◽  
Weidong Wang ◽  
Ira Kurtz ◽  
Jørgen Frøkiær ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Rat Kidney ◽  
Free Access ◽  
Thick Ascending Limb ◽  
Acid Base Balance ◽  
Acid Base ◽  
Chronic Metabolic Acidosis ◽  
Daily Water Intake ◽  
Base Balance ◽  
Access To Water

Several members of the Na-HCO[Formula: see text] cotransporter (NBC) family have recently been identified functionally and partly characterized, including rkNBC1, NBCn1, and NBC3. Regulation of these NBCs may play a role in the maintenance of intracellular pH and in the regulation of renal acid-base balance. However, it is unknown whether the expressions of these NBCs are regulated in response to changes in acid-base status. We therefore tested whether chronic metabolic acidosis (CMA) affects the abundance of these NBCs in kidneys using two conventional protocols. In protocol 1, rats were treated with NH4Cl in their drinking water (12 ± 1 mmol · rat−1 · day−1) for 2 wk with free access to water ( n = 8). Semiquantitative immunoblotting demonstrated that whole kidney abundance of NBCn1 and NBC3 in rats with CMA was dramatically increased to 995 ± 87 and 224 ± 35%, respectively, of control levels ( P < 0.05), whereas whole kidney rkNBC1 was unchanged (88 ± 14%). In protocol 2, rats were given NH4Cl in their food (10 ± 1 mmol · rat−1 · day−1) for 7 days, with a fixed daily water intake ( n = 6). Consistent with protocol 1, whole kidney abundances of NBCn1 (262 ± 42%) and NBC3 (160 ± 31%) were significantly increased compared with controls ( n = 6), whereas whole kidney rkNBC1 was unchanged (84 ± 17%). In both protocols, immunocytochemistry confirmed upregulation of NBCn1 and NBC3 with no change in the segmental distribution along the nephron. Consistent with the increase in NBCn1, measurements of pH transients in medullary thick ascending limb (mTAL) cells in kidney slices revealed two- to threefold increases in DIDS- sensitive, Na+-dependent HCO[Formula: see text] uptake in rats with CMA. In conclusion, CMA is associated with a marked increase in the abundance of NBCn1 in the mTAL and NBC3 in intercalated cells, whereas the abundance of NBC1 in the proximal tubule was not altered. The increased abundance of NBCn1 may play a role in the reabsorption of NH[Formula: see text] in the mTAL and increased NBC3 in reabsorbing HCO[Formula: see text].

Effects of acid-base disturbances on renal handling of magnesium in the dog

1986 ◽  
Vol 70 (3) ◽  
pp. 277-284 ◽  
Author(s):  
Norman L. M. Wong ◽  
Gary A. Quamme ◽  
John H. Dirks
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Indirect Effect ◽  
Metabolic Alkalosis ◽  
Distal Tubule ◽  
Acid Base ◽  
Renal Handling ◽  
Chronic Metabolic Acidosis ◽  
Magnesium Transport

1. Clearance and micropuncture studies were performed in four groups of acutely thyropara-thyroidectomized animals to study the effects of alkalosis and acidosis on the renal handling of magnesium. 2. Our results indicate that chronic metabolic acidosis reduces, whereas acute metabolic alkalosis enhances, magnesium reabsorption. 3. The site within the nephron where absorption of magnesium increases or decreases during acid-base disturbances was beyond the late proximal tubule. 4. Tubular fluid bicarbonate was also measured in these experiments, and the results indicated that magnesium reabsorption in the distal tubule correlated to bicarbonate delivery. However, whether this was a direct or an indirect effect of bicarbonate on magnesium transport could not be delineated.

Pendrin in the mouse kidney is primarily regulated by Cl− excretion but also by systemic metabolic acidosis

2008 ◽  
Vol 295 (6) ◽  
pp. C1658-C1667 ◽  
Author(s):  
Patricia Hafner ◽  
Rosa Grimaldi ◽  
Paola Capuano ◽  
Giovambattista Capasso ◽  
Carsten A. Wagner
Keyword(s):  
Metabolic Acidosis ◽  
Collecting Duct ◽  
Relative Number ◽  
High Protein ◽  
Acid Excretion ◽  
Acid Base ◽  
Urinary Acidification ◽  
Apical Side ◽  
Acid Base Status ◽  
Net Acid Excretion

The Cl−/anion exchanger pendrin (SLC26A4) is expressed on the apical side of renal non-type A intercalated cells. The abundance of pendrin is reduced during metabolic acidosis induced by oral NH4Cl loading. More recently, it has been shown that pendrin expression is increased during conditions associated with decreased urinary Cl− excretion and decreased upon Cl− loading. Hence, it is unclear if pendrin regulation during NH4Cl-induced acidosis is primarily due the Cl− load or acidosis. Therefore, we treated mice to increase urinary acidification, induce metabolic acidosis, or provide an oral Cl− load and examined the systemic acid-base status, urinary acidification, urinary Cl− excretion, and pendrin abundance in the kidney. NaCl or NH4Cl increased urinary Cl− excretion, whereas (NH4)2SO4, Na2SO4, and acetazolamide treatments decreased urinary Cl− excretion. NH4Cl, (NH4)2SO4, and acetazolamide caused metabolic acidosis and stimulated urinary net acid excretion. Pendrin expression was reduced under NaCl, NH4Cl, and (NH4)2SO4 loading and increased with the other treatments. (NH4)2SO4 and acetazolamide treatments reduced the relative number of pendrin-expressing cells in the collecting duct. In a second series, animals were kept for 1 and 2 wk on a low-protein (20%) diet or a high-protein (50%) diet. The high-protein diet slightly increased urinary Cl− excretion and strongly stimulated net acid excretion but did not alter pendrin expression. Thus, pendrin expression is primarily correlated with urinary Cl− excretion but not blood Cl−. However, metabolic acidosis caused by acetazolamide or (NH4)2SO4 loading prevented the increase or even reduced pendrin expression despite low urinary Cl− excretion, suggesting an independent regulation by acid-base status.

scholarly journals Acid-Base and Ionic Regulation in the American Eel (Anguilla Rostrata) During and after Prolonged Aerial Exposure: Branchial and Renal Adjustments

1987 ◽  
Vol 133 (1) ◽  
pp. 429-447 ◽  
Author(s):  
D. A. HYDE ◽  
S. F. PERRY
Keyword(s):  
Urine Flow ◽  
Anguilla Rostrata ◽  
Acid Excretion ◽  
Aerial Exposure ◽  
Acid Base ◽  
American Eel ◽  
Air Exposure ◽  
Extracellular Compartment ◽  
Acid Load ◽  
Pronounced Reduction

To whom reprint request should be addressed. The involvement of the gill and kidney in acid-base regulation was examined in the American eel, Anguilla rostrata, during 36h of continuous air-exposure and subsequent return to water. While in air, eels developed a severe mixed respiratory/- metabolic acidosis. Renal acid excretion increased only slightly during the latter stages of air-exposure. A pronounced reduction in urine flow rate was important to minimize dehydration but essentially eliminated the kidney as a route for excess acid excretion. Upon return to the water, eels had accrued an extracellular metabolic acid load of 9.53 mmol 1−1. The metabolic acid was cleared from the extracellular compartment at an exceptionally low rate (approximately 70μmol kg−1 h−1) and about 50 % of the acid load remained after 18 h of recovery in water. The clearance of metabolic acid was accounted for by enhanced branchial acid excretion which was related primarily to adjustments of unidirectional Na+ fluxes. Unidirectional Cl− fluxes were undetectable using radiotracer methods. We speculate that the inefficiency of acid-base regulation in the eel compared to other teleosts is, in part, related to the absence of significant branchial C1−/HCO3− exchange.

Effect of anaesthesia on insulin-induced hypoglycemia in rabbits

1988 ◽  
Vol 66 (12) ◽  
pp. 1531-1537 ◽  
Author(s):  
Fred J. Haynes ◽  
Surinder Cheema-Dhadli ◽  
Ross M. Halperin ◽  
Randy Zettle ◽  
Lisa Robinson ◽  
...  
Keyword(s):  
Energy Source ◽  
Oxygen Consumption ◽  
Glucose Oxidation ◽  
Lactate Concentration ◽  
Hepatic Glycogen ◽  
Rapid Rate ◽  
Energy Turnover ◽  
Rate Of Oxygen Consumption ◽  
Principal Energy ◽  
Insulin Overdose

The aim of this study was to determine how anaesthetized rabbits survive much longer than awake rabbits after receiving an insulin overdose. Insulin appeared to act in both groups of rabbits because there was a prompt fall in circulating glucose, free fatty acids, and β-hydroxybutyrate concentrations. Carbohydrate appeared to be the principal energy source for anaesthetized rabbits because their respiratory quotient approached unity. Although the fall in glycemia was similar in both groups of rabbits, the circulating lactate concentration rose only in the anaesthetized group. This rise in lactate in the initial 60 min after insulin was given could account for most of the fall in glycemia if the source of lactate was the glucose pool. The decline in hepatic glycogen was close to 100 μmol/g liver; this would account for about one-third of the total energy turnover and close to one-half of the measured glucose appearance in these anaesthetized rabbits. As judged from the rate of oxygen consumption, muscle glycogen seemed to supply two-thirds of the fuel to be oxidized in these rabbits. However, only one-third of the lactate released from muscle was first converted to glucose and the remainder was oxidized directly to CO2. Although insulin provided the metabolic setting for a rapid rate of glucose oxidation, this rate appeared to be diminished when the overall rate of oxygen consumption was lower during anaesthesia.

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