Renal function and acid–base regulation in two Amazonian erythrinid fishes: Hoplias malabaricus, a water breather, and Hoplerythrinus unitaeniatus, a facultative air breather

1978 ◽  
Vol 56 (4) ◽  
pp. 917-930 ◽  
Author(s):  
James N. Cameron ◽  
Chris M. Wood
Keyword(s):  
Ammonia Excretion ◽  
Titratable Acidity ◽  
Acid Excretion ◽  
Acid Base ◽  
Total Acid ◽  
Urine Ph ◽  
Air Breathing ◽  
Hoplias Malabaricus ◽  
Urinary Parameters ◽  
Hoplerythrinus Unitaeniatus

The function of the kidney in ion, water, and acid excretion was investigated in two erythrinid fishes, the water-breathing Hoplias malabaricus and the facultative air-breathing Hoplerythrinus unitaeniatus. Chronic catheterization of the urinary papilla and the dorsal aorta provided information on the urinary parameters and blood acid–base status. By monitoring total flow of urine, pH, and concentrations of Na+, Cl−, ammonia, titratable acidity, and lactate, the total renal flux of water, various ions, and total acid was computed. The kidneys of both species were found capable of acidifying urine, creating gradients of up to 620:1 for H+ ion, and contributing substantially to steady-state acid excretion. There was no significant increase in lactate or total acid efflux from urine during postoperative (metabolic) acidosis. Respiratory (hypercapnic) acidosis caused a compensatory increase in blood HCO3−, and an increase in branchial Na+ uptake (presumably by Na–H exchange), but no change in ammonia excretion. There was no renal response in one Hoplias to hypercapnia, but an increased acid excretion in one Hoplerythrinus. The behavior of the urinary excretion system appears in various respects similar to the higher vertebrates. There was no obvious correlation between renal parameters and air breathing in these two species.

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.

Role of organic anions in renal response to dietary acid and base loads

1989 ◽  
Vol 257 (2) ◽  
pp. F170-F176 ◽  
Author(s):  
J. C. Brown ◽  
R. K. Packer ◽  
M. A. Knepper
Keyword(s):  
Organic Anion ◽  
Organic Anions ◽  
Acid Excretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Urine Ph ◽  
Renal Response ◽  
Base Balance ◽  
Net Acid Excretion

Bicarbonate is formed when organic anions are oxidized systemically. Therefore, changes in organic anion excretion can affect systemic acid-base balance. To assess the role of organic anions in urinary acid-base excretion, we measured urinary excretion in control rats, NaHCO3-loaded rats, and NH4Cl-loaded rats. Total organic anions were measured by the titration method of Van Slyke. As expected, NaHCO3 loading increased urine pH and decreased net acid excretion (NH4+ + titratable acid - HCO3-), whereas NH4Cl loading had the opposite effect. Organic anion excretion was increased in response to NaHCO3 loading and decreased in response to NH4Cl loading. We quantified the overall effect of organic ion plus inorganic buffer ion excretion on acid-base balance. The amounts of organic anions excreted by all animals in this study were greater than the amounts of NH4+, HCO3-, or titratable acidity excreted. In addition, in response to acid and alkali loading, changes in urinary organic anion excretion were 40-50% as large as changes in net acid excretion. We conclude that, in rats, regulation of organic anion excretion can contribute importantly to the overall renal response to acid-base disturbances.

Acid excretion by bicarbonate-free perfused rat kidney

1981 ◽  
Vol 240 (4) ◽  
pp. F306-F310
Author(s):  
M. H. Garvey ◽  
D. L. Maude
Keyword(s):  
Carbonic Anhydrase ◽  
Rat Kidney ◽  
Acid Excretion ◽  
Total Acid ◽  
Urine Ph ◽  
Titratable Acid ◽  
Perfused Rat Kidney ◽  
Reduced Rate ◽  
Isolated Rat

We measured titratable acid (TA) and NH4 excretion by isolated rat kidneys perfused either with conventional bicarbonate-containing solutions or with solutions in which bicarbonate was replaced by propionate. Rates of TA excretion by bicarbonate-perfused kidneys were similar to in vivo values, 0.27 +/- 0.04 mueq.ml GF-1 (0.21 mueq.min-1.g-1), and increased significantly under bicarbonate-free conditions to 0.70 +/- 0.12 mueq.ml GF-1 (0.42 mueq.min-1.g-1). At the same time the perfusate/urine pH difference (delta pH) increased significantly, from 0.63 +/- 0.06 to 0.92 +/- 0.06. Carbonic anhydrase inhibition by 5 X 10(-4) M acetazolamide alkalinized the urine of bicarbonate-perfused kidneys, while in the bicarbonate-free preparation the urine remained acid (delta pH = 0.27 +/- 0.04) and titratable acid continued to be excreted, though at a reduced rate, 0.19 +/- 0.04 mueq.ml GF-1. Under these same bicarbonate-free carbonic anhydrase-inhibited conditions, lowering the perfusate pH from 7.4 to 7.1 increased delta pH to 0.36 +/- 0.02 and caused total acid excretion (TA + NH4) to rise from 0.29 +/- 0.04 to 0.45 +/- 0.06 mueq.ml GF-1, and increasing the perfusate [HPO4] from 2.4 to 9.6 mM increased TA to 0.80 +/- 0.09 mueq.ml GF-1.

Some kinetic properties of skeletal muscle pyruvate kinase from air-breathing and water-breathing fish of the Amazon

1978 ◽  
Vol 56 (4) ◽  
pp. 751-758 ◽  
Author(s):  
J. H. A. Fields ◽  
W. R. Driedzic ◽  
C. J. French ◽  
P. W. Hochachka
Keyword(s):  
Skeletal Muscle ◽  
Pyruvate Kinase ◽  
Adenosine Diphosphate ◽  
Kinetic Properties ◽  
Air Breathing ◽  
Hoplias Malabaricus ◽  
Arapaima Gigas ◽  
Saturation Kinetics ◽  
Muscle Pyruvate Kinase ◽  
Hoplerythrinus Unitaeniatus

The kinetic properties of pyruvate kinase from skeletal muscle were studied in two species of air-breathing fish, Hoplerythrinus unitaeniatus and Arapaima gigas, and two species of water-breathing fish, Hoplias malabaricus and Osteoglossum bicirrhosum. It was found that the enzymes from Hoplias and Hoplerythrinus showed hyperbolic saturation kinetics for all substrates, were activated slightly by fructose 1,6-diphosphate, and were inhibited by phosphocreatine and citrate. The enzyme from Hoplias was inhibited by alanine, whereas the enzyme from Hoplerythrinus was not. The enzymes from Arapaima and Osteoglossum showed hyperbolic saturation kinetics for adenosine diphosphate, but the saturation kinetics for phusphoenol-pyruvate were sigmoidal. These enzymes were strongly activated by fructose 1,6-diphosphate and strongly inhibited by alanine, the former completely reversing the inhibition by the latter. Phosphocreatine and citrate were also found to be inhibitors of these enzymes, but the inhibition by phosphocreatine was not reversed by additions of fructose 1,6-diphosphate. The enzymes from the water-breathing fish were more sensitive to inhibition by alanine than were those from the air-breathing fish, but in other respects the enzymes were very similar.

Effects of glucocorticoid steroids on renal and systemic acid-base metabolism

1980 ◽  
Vol 239 (1) ◽  
pp. F30-F43 ◽  
Author(s):  
H. N. Hulter ◽  
J. H. Licht ◽  
E. L. Bonner ◽  
R. D. Glynn ◽  
A. Sebastian
Keyword(s):  
Steady State ◽  
Acid Production ◽  
Chronic Administration ◽  
Acid Excretion ◽  
Acid Base ◽  
Unmeasured Anion ◽  
Urine Ph ◽  
Group I ◽  
Potassium Clearance ◽  
Net Acid Excretion

Clinical states of hyperglucocorticoidism are associated with renal metabolic alkalosis, yet the systemic and renal acid-base response to chronic administration of glucocorticoid steroids (dexamethasone, triamcinolone) possessing little or no mineralocorticoid activity has not been investigated. In balance studies studies in dogs administration of triamcinolone (Tcn), 1.0 mg. kg-1. day-1 for 6–9 days (group I, n = 5), resulted in a persistent reduction in urine pH and increase in net acid excretion (NAE), and in the excretion of urinary unmeasured anions (C+NH4,Na;K minus A-Cl,HCO3,Pi), which were identified as organic anions and sulfate. A significant degree of metabolic acidosis occurred initially (delta [HCO3-]p, -3.4 meq/liter, P less than 0.05, day 1). As Tcn administration was continued, the cumulative increment in net acid excreted exceeded the cumulative increment in urinary unmeasured anion excreted and [HCO-3]p returned to pre-Tcn control values and remained stable thereafter. In the steady state of Tcn administration plasma potassium concentration and renal potassium clearance were not significantly different from pre-Tcn control, in contrast to the findings of hypokalemia and increased renal potassium clearance during chronic administration of deoxycorticosterone (DOC). Triamcinolone did not result in antinatriuresis or antichloruresis. Chronic administration of a 10–fold smaller dose of Tcn (0.1 mg . kg-1 . day-1) in an additional group (group III) also resulted in a persisting reduction in urine pH and an increase in net acid excretion that exceeded unmeasured anion excretion and resulted in a small increase in steady-state plasma bicarbonate concentration. These results suggest that chronic administration of potent glucocorticoid steroids results in 1) a persisting increase in endogenous acid production, and 2) stimulation of renal hydrogen ion secretion that was of greater degree than accounted for by the increment in endogenous acid production and that was not accompanied by renal mineralocorticoid effects on sodium and potassium transport.

Kidney Glutaminase and Carbonic Anhydrase Activities and Renal Electrolyte Excretion in Rats

1955 ◽  
Vol 184 (1) ◽  
pp. 83-90 ◽  
Author(s):  
Edward Muntwyler ◽  
Michael Iacobellis ◽  
Grace E. Griffin
Keyword(s):  
Carbonic Anhydrase ◽  
Ammonia Excretion ◽  
Titratable Acidity ◽  
Carbonic Anhydrase Activity ◽  
Chemical Compositions ◽  
Electrolyte Excretion ◽  
Urine Ph ◽  
K Deficiency ◽  
Renal Carbonic Anhydrase ◽  
Glutaminase Activity

The plasma electrolyte composition and 24-hour urine electrolyte excretion were determined in fasting normal, K-deficient and protein and K-deficient rats following the administration of equal molar quantities of NaCl, KCl, NH4Cl and KHCO3. An attempt was made to relate any differences in the compositions of the plasma and urine to the levels of renal glutaminase and carbonic anhydrase activities, and, to the chemical compositions of the skeletal muscle and kidneys. Renal glutaminase and carbonic anhydrase activities were found increased in K-deficiency and reduced in protein and K-deficiency. Significant changes from corresponding control levels of renal glutaminase were found in normal and K-deficient animals only after the administration of NH4Cl (increased), and, after the administration of KHCO3 (reduced). The only outstanding change of the carbonic anhydrase activity of the kidneys from these animals was a reduction following NH4Cl administration. The doubly deficient rats showed a significant increase in renal glutaminase activity after NH4Cl administration; on the other hand, KCl administration resulted in a further reduction of the lowered renal carbonic anhydrase activity. The experimental results supported the contention that a relationship exists between urinary ammonia excretion and the level of renal glutaminase activity, while the transfer of H+ to the urine and the level of renal carbonic anhydrase activity could not be related. No clear relationship was found between the K excretion and/or K content of the kidneys and the urine total titratable acidity and ammonia excretion, and urine ph.

Handling of ammonium by the renal proximal tubule during acute metabolic acidosis

1983 ◽  
Vol 245 (6) ◽  
pp. F680-F686 ◽  
Author(s):  
E. Simon ◽  
D. Martin ◽  
J. Buerkert
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Acid Excretion ◽  
Total Acid ◽  
Urine Ph ◽  
Acid Infusion ◽  
Acute Metabolic Acidosis ◽  
Fluid Collections ◽  
Tubule Fluid

The present studies were designed to assess the handling of ammonium (NH+4) by the proximal tubule during acute metabolic acidosis (AMA). After tubule fluid collections were obtained with micropuncture techniques and in situ pH was determined near the end of the proximal tubule, 0.2 N HCl was infused intravenously at 17 microliter X min-1 X 100 g body wt-1. Thirty to sixty minutes later, samples were obtained and pH measurements were made near the previous micropuncture sites. During AMA, urine pH fell and total acid excretion doubled due to an increase in NH+4 excretion from 581 +/- 63 to 1,153 +/- 61 nmol X min-1 X g kidney wt-1 (P less than 0.001). Acid excretion did not change in time controls. Tubule fluid NH+4 rose from 2.17 +/- 0.15 to 3.45 +/- 0.24 mM during acid infusion (P less than 0.001) and its delivery to the end of the proximal tubule nearly doubled (67.8 +/- 6.3 vs. 33.9 +/- 2.9 pmol X min X g kidney wt-1 before acid infusion, P less than 0.001). This increase in delivery during AMA was due to enhanced ammonia (NH3) entry into the proximal tubule. In situ pH determined near the end of the proximal tubule averaged 6.94 +/- 0.04 before acid infusion and did not change afterwards (6.87 +/- 0.05). These data are consistent with the hypothesis that in AMA the increase in NH+4 excretion is due primarily to an increase in the cortical production of NH3.

scholarly journals Role of the Rhesus glycoprotein, Rh B glycoprotein, in renal ammonia excretion

2010 ◽  
Vol 299 (5) ◽  
pp. F1065-F1077 ◽  
Author(s):  
Jesse M. Bishop ◽  
Jill W. Verlander ◽  
Hyun-Wook Lee ◽  
Raoul D. Nelson ◽  
Arthur J. Weiner ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Glutamine Synthetase ◽  
Collecting Duct ◽  
Ammonia Excretion ◽  
Acid Excretion ◽  
Urine Ph ◽  
Outer Medulla ◽  
Intercalated Cell ◽  
Titratable Acid ◽  
Acid Loading

Rh B glycoprotein (Rhbg) is a member of the Rh glycoprotein family of ammonia transporters. In the current study, we examine Rhbg's role in basal and acidosis-stimulated acid-base homeostasis. Metabolic acidosis induced by HCl administration increased Rhbg expression in both the cortex and outer medulla. To test the functional significance of increased Rhbg expression, we used a Cre-loxP approach to generate mice with intercalated cell-specific Rhbg knockout (IC-Rhbg-KO). On normal diet, intercalated cell-specific Rhbg deletion did not alter urine ammonia excretion, pH, or titratable acid excretion significantly, but it did decrease glutamine synthetase expression in the outer medulla significantly. After metabolic acidosis was induced, urinary ammonia excretion was significantly less in IC-Rhbg-KO than in control (C) mice on days 2–4 of acid loading, but not on day 5. Urine pH and titratable acid excretion and dietary acid intake did not differ significantly between acid-loaded IC-Rhcg-KO and C mice. In IC-Rhbg-KO mice, acid loading increased connecting segment (CNT) cell and outer medullary collecting duct principal cell Rhbg expression. In both C and IC-Rhbg-KO mice, acid loading decreased glutamine synthetase in both the cortex and outer medulla; the decrease on day 3 was similar in IC-Rhbg-KO and C mice, but on day 5 it was significantly greater in IC-Rhbg-KO than in C mice. We conclude 1) intercalated cell Rhbg contributes to acidosis-stimulated renal ammonia excretion, 2) Rhbg in CNT and principal cells may contribute to renal ammonia excretion, and 3) decreased glutamine synthetase expression may enable normal rates of ammonia excretion under both basal conditions and on day 5 of acid loading in IC-Rhbg-KO mice.

scholarly journals Ammonia Transporters and Their Role in Acid-Base Balance

2017 ◽  
Vol 97 (2) ◽  
pp. 465-494 ◽  
Author(s):  
I. David Weiner ◽  
Jill W. Verlander
Keyword(s):  
Ammonia Excretion ◽  
Transport Processes ◽  
Molecular Forms ◽  
Acid Excretion ◽  
Acid Base ◽  
Titratable Acid ◽  
Renal Net Acid Excretion ◽  
Ammonia Transport ◽  
Specific Proteins ◽  
Net Acid Excretion

Acid-base homeostasis is critical to maintenance of normal health. Renal ammonia excretion is the quantitatively predominant component of renal net acid excretion, both under basal conditions and in response to acid-base disturbances. Although titratable acid excretion also contributes to renal net acid excretion, the quantitative contribution of titratable acid excretion is less than that of ammonia under basal conditions and is only a minor component of the adaptive response to acid-base disturbances. In contrast to other urinary solutes, ammonia is produced in the kidney and then is selectively transported either into the urine or the renal vein. The proportion of ammonia that the kidney produces that is excreted in the urine varies dramatically in response to physiological stimuli, and only urinary ammonia excretion contributes to acid-base homeostasis. As a result, selective and regulated renal ammonia transport by renal epithelial cells is central to acid-base homeostasis. Both molecular forms of ammonia, NH3 and NH4+, are transported by specific proteins, and regulation of these transport processes determines the eventual fate of the ammonia produced. In this review, we discuss these issues, and then discuss in detail the specific proteins involved in renal epithelial cell ammonia transport.

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