scholarly journals Ca2+-driven intestinal HCO3− secretion and CaCO3 precipitation in the European flounder in vivo: influences on acid-base regulation and blood gas transport

2010 ◽  
Vol 298 (4) ◽  
pp. R870-R876 ◽  
Author(s):  
Christopher A. Cooper ◽  
Jonathan M. Whittamore ◽  
Rod W. Wilson
Keyword(s):  
Teleost Fish ◽  
Gas Transport ◽  
Driving Forces ◽  
Marine Teleost ◽  
Acid Excretion ◽  
Acid Base ◽  
Marine Teleost Fish ◽  
Net Acid Excretion

Marine teleost fish continuously ingest seawater to prevent dehydration and their intestines absorb fluid by mechanisms linked to three separate driving forces: 1) cotransport of NaCl from the gut fluid; 2) bicarbonate (HCO3−) secretion and Cl− absorption via Cl−/HCO3− exchange fueled by metabolic CO2; and 3) alkaline precipitation of Ca2+ as insoluble CaCO3, which aids H2O absorption). The latter two processes involve high rates of epithelial HCO3− secretion stimulated by intestinal Ca2+ and can drive a major portion of water absorption. At higher salinities and ambient Ca2+ concentrations the osmoregulatory role of intestinal HCO3− secretion is amplified, but this has repercussions for other physiological processes, in particular, respiratory gas transport (as it is fueled by metabolic CO2) and acid-base regulation (as intestinal cells must export H+ into the blood to balance apical HCO3− secretion). The flounder intestine was perfused in vivo with salines containing 10, 40, or 90 mM Ca2+. Increasing the luminal Ca2+ concentration caused a large elevation in intestinal HCO3− production and excretion. Additionally, blood pH decreased (−0.13 pH units) and plasma partial pressure of CO2 (Pco2) levels were elevated (+1.16 mmHg) at the highest Ca perfusate level after 3 days of perfusion. Increasing the perfusate [Ca2+] also produced proportional increases in net acid excretion via the gills. When the net intestinal flux of all ions across the intestine was calculated, there was a greater absorption of anions than cations. This missing cation flux was assumed to be protons, which vary with an almost 1:1 relationship with net acid excretion via the gill. This study illustrates the intimate link between intestinal HCO3− production and osmoregulation with acid-base balance and respiratory gas exchange and the specific controlling role of ingested Ca2+ independent of any other ion or overall osmolality in marine teleost fish.

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-BASE REGULATION, BRANCHIAL TRANSFERS AND RENAL OUTPUT IN A MARINE TELEOST FISH (THE LONG-HORNED SCULPIN MYOXOCEPHALUS OCTODECIMSPINOSUS) DURING EXPOSURE TO LOW SALINITIES

1994 ◽  
Vol 193 (1) ◽  
pp. 79-95 ◽  
Author(s):  
J Claiborne ◽  
J Walton ◽  
D Compton-Mccullough
Keyword(s):  
Teleost Fish ◽  
Sea Water ◽  
Carbon Dioxide Concentration ◽  
Marine Teleost ◽  
Total Acid ◽  
Low Salinity ◽  
External Salinity ◽  
First Time ◽  
Marine Teleost Fish

A number of studies have implied a linkage between acid­base and ion exchanges in both freshwater and seawater fish, although little is known about the branchial and renal acid­base transfers involved as the animals move between different salinities. To investigate the role of these transfers in a marine teleost fish as it is exposed to a dilute environment, we measured plasma acid­base values and net movements from fish to water of NH4+, HCO3- and H+ in long-horned sculpin (Myoxocephalus octodecimspinosus) placed in 100 %, 20 %, 8 % or 4 % sea water for 24­48 h. Renal excretion of H+ was also monitored in fish exposed to 4 % sea water. Sculpin proved to be somewhat euryhaline for they were able to maintain plasma ion and acid­base transfers in hypo-osmotic (20 %) sea water, but could not tolerate greater dilutions for more than several days. Plasma pH and carbon dioxide concentration (CCO2) increased in the 20 % and 8 % dilution groups, with CCO2 nearly doubling (control, 4.56 mmol l-1; 8 % group, 8.56 mmol l-1) as a result of a combined increase in the partial pressure of plasma CO2 (PCO2) and [HCO3-]. During a 44­46 h exposure, HCO3- transfers increased progressively in the most dilute water, with animals in the 8 % and 4 % groups exhibiting a net H+ loss that was smaller than that of seawater fish (control, 5.1 mmol kg-1; 8 %, 0.9 mmol kg-1; 4 %, -2.9 mmol kg-1). Animals exposed to 4 % sea water for 24 h and then returned to normal sea water had a variable plasma pH, an elevated CCO2 and a net efflux of H+ that effectively stopped (control, 0.10 mmol kg-1 h-1; 4 %, 0.02 mmol kg-1 h-1; seawater recovery, 0.20 mmol kg-1 h-1) during the low-salinity period. Renal acid excretion remained relatively constant throughout the experiment but only made up a significant portion (approximately 40 %) of the total acid transfers during the 4 % dilution period (control rate approximately 3 µmol kg-1 h-1: 3 % of branchial rate). We postulate that the increase in plasma CCO2 during exposure to low salinity may be due to mobilization of base from the intracellular bone compartment. The decrease in external salinity could induce base loss by alteration of gill ion exchanges (Na+/H+, Cl-/HCO3-) and/or changes in branchial HCO3- permeability. For the first time, we have shown that the effects of a dilute environment on acid­base transfers may be an important limitation to the survival of a euryhaline species in brackish or fresh water.

Role of citrate excretion in acid-base balance in diuretic-induced alkalosis in the rat

1985 ◽  
Vol 248 (6) ◽  
pp. F796-F803 ◽  
Author(s):  
A. M. Kaufman ◽  
C. Brod-Miller ◽  
T. Kahn
Keyword(s):  
Base Line ◽  
Acid Excretion ◽  
Acid Base Balance ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Base Balance ◽  
Furosemide Administration ◽  
Net Acid Excretion

Studies were performed to assess the role of changes in the excretion of citrate, a metabolic precursor of bicarbonate, in acid-base balance in diuretic-induced metabolic alkalosis. Rats on a low-chloride diet with sodium sulfate added were studied during a base-line period, 3 days of furosemide administration, and 4 days post-furosemide. During the period of furosemide administration, net acid excretion and plasma bicarbonate concentration increased. In the post-furosemide period, net acid excretion remained higher than base line but plasma bicarbonate concentration did not increase further. Citrate excretion was significantly higher in the post-furosemide period than in base line. Studies substituting sodium neutral phosphate or sodium bicarbonate for dietary sodium sulfate demonstrated greater increases in net acid excretion post-furosemide and, again, no increase in plasma bicarbonate concentration during this period. Citrate excretion was greater than in the sulfate group. The increment in citrate excretion was proportional to the base “load,” defined with respect to changes in net acid excretion and/or dietary bicarbonate. Thus, in these studies alterations of base excretion in the form of citrate play an important role in acid-base balance during diuretic-induced metabolic alkalosis.

Potassium-depletion alkalosis in the rat

1988 ◽  
Vol 255 (4) ◽  
pp. F763-F770 ◽  
Author(s):  
A. M. Kaufman ◽  
T. Kahn
Keyword(s):  
Potassium Depletion ◽  
Base Line ◽  
Acid Excretion ◽  
Acid Base ◽  
Deficient Diet ◽  
Chloride Depletion ◽  
Acid Load ◽  
The Relationship ◽  
Net Acid Excretion

Studies were performed to investigate the role of concomitant chloride depletion in potassium-depletion alkalosis in the rat and the relationship between potassium depletion, plasma bicarbonate (PHCO3), and net acid excretion. 1) Selective potassium depletion (K-DEPL), potassium plus chloride depletion (KCl-DEPL), or selective chloride depletion (Cl-DEPL) was produced by administering a selectively potassium-, potassium and chloride-, or selectively chloride-deficient diet. In K-DEPL and KCl-DEPL rat, PHCO3 increased progressively and similarly during a 38-day period of restriction, whereas net acid excretion was similar and not elevated in either group. Cl-DEPL did not result in alkalosis. Chloride administration without potassium in alkalotic KCl-DEPL rats did not result in a sustained significant decrease in PHCO3. Potassium administration without chloride in alkalotic KCl-DEPL rats decreased PHCO3. Thus concomitant chloride depletion plays a minimal role in the alkalosis produced by dietary-induced potassium depletion. 2) Administration of a chronic acid load to alkalotic K-DEPL rats did not decrease PHCO3, and net acid excretion increased similarly as in normals. In K-DEPL rats after PHCO3 was reduced toward normal levels with acetazolamide, net acid excretion increased sharply above base-line values and PHCO3 increased markedly. Thus the alkalotic K-DEPL rat maintains the ability to excrete a chronic acid load, and a reduction in PHCO3 elicits an increase in acid excretion to restore the initial acid-base condition. These studies suggest that potassium depletion alters the set-point at which the kidney maintains PHCO3.

Role of ion transfer processes in acid-base regulation with temperature changes in fish

1984 ◽  
Vol 246 (4) ◽  
pp. R441-R451 ◽  
Author(s):  
N. Heisler
Keyword(s):  
Ion Transfer ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Fish Tissues ◽  
Model Calculations ◽  
Temperature Changes ◽  
Transfer Processes ◽  
Transfer Mechanisms

The contributions of transmembrane and transepithelial ion transfer processes and of nonbicarbonate buffering to the in vivo acid-base regulation have been evaluated. Model calculations were performed utilizing experimental data on transepithelial transfer of ions relevant for the acid-base regulation, the intracellular buffering properties of fish tissues, and the behavior of intracellular and extracellular pH and bicarbonate concentration with changes of temperature. The results of these studies indicate that the changes in the pK values of physiological nonbicarbonate buffers with changes in temperature support the adjustment of pH to lower values with rising temperature; however, transmembrane and transepithelial ion transfer mechanisms determine the acid-base regulation of intracellular and extracellular compartments.

Oil Spill Dispersant Use: Toxicity on Marine Teleost Fish

2018 ◽  
pp. 71-82
Author(s):  
Thomas Milinkovitch ◽  
Stéphane Le Floch ◽  
Hélène Thomas-Guyon
Keyword(s):  
Oil Spill ◽  
Teleost Fish ◽  
Marine Teleost ◽  
Marine Teleost Fish

Deoxycorticosterone-stimulated bicarbonate secretion in rabbit cortical collecting ducts: effects of luminal chloride removal and in vivo acid loading

1985 ◽  
Vol 249 (2) ◽  
pp. F205-F212 ◽  
Author(s):  
J. Garcia-Austt ◽  
D. W. Good ◽  
M. B. Burg ◽  
M. A. Knepper
Keyword(s):  
Collecting Duct ◽  
High Rate ◽  
Bicarbonate Secretion ◽  
Cortical Collecting Duct ◽  
Acid Base ◽  
Urinary Ph ◽  
Collecting Ducts ◽  
Acid Loading

To assess the role of cortical collecting duct bicarbonate secretion in the regulation of net acid excretion, we have sought to identify what factors influence the secretion rate. Net and unidirectional bicarbonate fluxes were measured in isolated perfused cortical collecting ducts from deoxycorticosterone-treated rabbits. The collecting ducts secreted bicarbonate at 11-24 pmol X mm-1 X min-1, confirming the high rate seen in earlier studies. Oral acid loading (50 mM NH4Cl drinking water) completely inhibited the net bicarbonate secretion. The bath-to-lumen flux was markedly reduced with acid loading, but the lumen-to-bath flux changed very little. In tubules from rabbits treated with deoxycorticosterone (but not NH4Cl), luminal chloride replacement with either sulfate or gluconate completely and reversibly inhibited the net bicarbonate secretion. The bath-to-lumen flux was greatly inhibited, but there was little change in the lumen-to-bath flux. We conclude: 1) High rates of bicarbonate secretion can be induced in rabbit cortical collecting ducts by chronic treatment of the animals with deoxycorticosterone. 2) When deoxycorticosterone-treated rabbits were made acidotic by oral administration of NH4Cl, the bicarbonate secretion was prevented, indicating that the systemic acid-base state of the animal may be an important factor regulating bicarbonate secretion. 3) Replacement of chloride in the lumen with sulfate inhibits bicarbonate secretion in the cortical collecting duct, an effect which may explain in part the decrease in urinary pH in response to sulfate infusions in mineralocorticoid-stimulated animals.

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