Survival, Acid-Base Regulation, Ion Regulation, and Ammonia Excretion in Rainbow Trout in Highly Alkaline Hard Water

1992 ◽  
Vol 65 (4) ◽  
pp. 763-787 ◽  
Author(s):  
Timothy Y. Yesaki ◽  
George K. Iwama
Keyword(s):  
Rainbow Trout ◽  
Ammonia Excretion ◽  
Hard Water ◽  
Acid Base ◽  
Ion Regulation

Branchial mechanisms of ion and acid–base regulation in the freshwater rainbow trout, Salmo gairdneri

1988 ◽  
Vol 66 (12) ◽  
pp. 2699-2708 ◽  
Author(s):  
D. G. McDonald ◽  
E. T. Prior
Keyword(s):  
Lactic Acid ◽  
Rainbow Trout ◽  
Sodium Bicarbonate ◽  
Ammonium Sulphate ◽  
Ammonia Excretion ◽  
Salmo Gairdneri ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance

Blood acid–base balance and branchial fluxes of Na+, Cl−, and acidic equivalents were examined in rainbow trout (Salmo gairdneri) in response to variations in external [NaCl] and following experimental acid or base loads (intravascular infusion of ammonium sulphate, lactic acid, or sodium bicarbonate). NaCl influx, NaCl efflux, and ammonia excretion covaried with external [NaCl]. Large fluxes of acidic equivalents across the gills were produced by infusion of both ammonium sulphate and sodium bicarbonate, but both treatments had little effect upon Na+ and Cl− uptake. We interpret this result as indicating that apical [Formula: see text] and [Formula: see text] exchange played little role in the branchial clearance of acidic equivalents. Instead, the results are consistent with the notion that acidic equivalents were excreted via diffusion through paracellular channels. A model is presented which suggests that the paracellular channels are the normal route for ionic efflux across the gills and that excretion of acidic equivalents results from modulation of the permselectivity of this pathway.

scholarly journals The effects of prolonged epinephrine infusion on the physiology of the rainbow trout, Salmo gairdneri. II. Branchial solute fluxes

1987 ◽  
Vol 128 (1) ◽  
pp. 255-267 ◽  
Author(s):  
M. G. Vermette ◽  
S. F. Perry
Keyword(s):  
Rainbow Trout ◽  
Ammonia Excretion ◽  
Salmo Gairdneri ◽  
Ionic Exchange ◽  
Acid Base ◽  
Epinephrine Infusion ◽  
Extracellular Acidosis ◽  
Titratable Acid ◽  
Solute Fluxes ◽  
Circulating Levels

Rainbow trout were infused continuously for 24 h with epinephrine in order to elevate circulating levels to those measured during periods of acute extracellular acidosis (about 5 X 10(−8) mol l-1). Concomitant effects on branchial solute fluxes were evaluated. Epinephrine infusion caused complex and differential adjustments of Na+ and Cl- unidirectional fluxes (influx and efflux) resulting in a significant elevation of the arithmetic difference between Na+ and Cl- net fluxes (JnetNa+-JnetCl-). A significant correlation existed between JnetNa+-JnetCl- and net branchial acid excretion (JnetH+), thereby suggesting a role for epinephrine in piscine acid-base regulation. The stimulation of JnetH+ by epinephrine was due primarily to a reduction in the excretion of titratable acid (JTA) accompanied by non-significant changes in ammonia excretion (JAmm). The results are discussed with respect to a role for epinephrine in regulating acid-base disturbances by interacting with branchial ionic exchange mechanisms.

scholarly journals Transbranchial ammonia gradients and acid-base responses to high external ammonia concentration in rainbow trout (Oncorhynchus mykiss) acclimated to different salinities

1992 ◽  
Vol 166 (1) ◽  
pp. 95-112 ◽  
Author(s):  
R. W. Wilson ◽  
E. W. Taylor
Keyword(s):  
Rainbow Trout ◽  
Sea Water ◽  
Ammonia Excretion ◽  
Ammonia Concentration ◽  
Acid Base ◽  
Experimental Conditions ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Total Ammonia ◽  
Acid Base Status ◽  
The Difference

Transbranchial ammonia gradients and blood acid-base status have been examined in rainbow trout acclimated to fresh water (FW), 33% sea water (33% SW) and sea water (SW) and exposed to 1.0 mmol l-1 total ammonia (TAmm) at pH 7.9 for 24 h. At all three salinities trout maintained large negative (inwardly directed) NH3 and NH4+ gradients throughout the exposure, presumably by active excretion of NH4+ to counteract the passive inward diffusion of ammonia. Analysis of blood non-respiratory acid-base status (delta H+m) revealed an acid load in FW trout and a base load in SW trout following 24 h of exposure. This indicates that active NH4+/H+ exchange predominates in FW whereas NH4+/Na+ is the principal exchange utilised in SW under these experimental conditions. The plasma TAmm load incurred during ammonia exposure increased with salinity. Compared to FW trout, plasma TAmm values were 34 and 73% higher in the 33% SW and SW trout, respectively, after 24 h. This cannot be explained by differences in the prevailing transbranchial PNH3 gradient because ambient PNH3 was substantially lower at the higher salinities (due to higher pK' and solubility values). We interpret the difference between FW and SW trout as an increased permeability to NH4+ in fish acclimated to the higher-salinity environments. Transbranchial diffusion of NH4+ is, therefore, probably more important as a route for ammonia excretion in SW than in FW trout, especially considering the favourable transepithelial potentials normally found in SW teleosts. In addition, increased NH4+ permeability implies that the toxicity of ammonia will be greater in seawater than in freshwater teleosts and should not simply be measured as a function of the unionised ammonia concentration when considering seawater-adapted species.

Ion Flux Rates, Acid–Base Status, and Blood Gases in Rainbow Trout, Salmo gairdneri, Exposed to Toxic Zinc in Natural Soft Water

1985 ◽  
Vol 42 (8) ◽  
pp. 1332-1341 ◽  
Author(s):  
Douglas J. Spry ◽  
Chris M. Wood
Keyword(s):  
Rainbow Trout ◽  
Metabolic Acidosis ◽  
Ammonia Excretion ◽  
Blood Gases ◽  
Soft Water ◽  
Salmo Gairdneri ◽  
Acid Base ◽  
Flux Measurements ◽  
Water Base ◽  
Toxic Concentrations

Exposure to 0.8 mg Zn2+/L in natural soft water for up to 72 h was toxic to rainbow trout, Salmo gairdneri, causing an acid–base disturbance and net branchial ion losses. Mean arterial pH fell from 7.78 to 7.58. Both [Formula: see text] and lactate rose, indicating a mixed respiratory and metabolic acidosis, despite maintenance of high [Formula: see text] Net branchial uptake of Na+ and Cl− became a net loss immediately following exposure to Zn2+, and this continued during 60 h of exposure. Net K+ loss was exacerbated, and net Ca2+ uptake was abolished. Unidirectional flux measurements with 22Na+ and 36Cl− indicated an increased efflux immediately following zinc exposure. Both influx and efflux of Na+ and Cl− were stimulated after 48–60 h in Zn2+. Both net branchial ammonia excretion and net branchial uptake of acidic equivalents from the water (=base loss) were greatly stimulated, the latter contributing to metabolic acidosis. Kidney function, as measured by urine flow rate and excretion of ammonia, acidic equivalents, Na+, Cl−, K+, and Zn2+, was relatively insensitive to the effects of zinc. The only renal component to be affected was Ca2+ excretion, which decreased during a single flux period, possibly in response to the reduced entry of Ca2+ at the gill. We conclude that toxic concentrations of zinc are capable of altering gill function so as to cause ionoregulatory and acid–base disturbances without disturbance of [Formula: see text].

Respiratory, Ventilatory, Acid-Base and Ionoregulatory Physiology of the White Sucker Catostomus Commersoni: The Influence of Hyperoxia

1981 ◽  
Vol 91 (1) ◽  
pp. 239-254
Author(s):  
P. R. H. Wilkes ◽  
R. L. Walker ◽  
D. G. McDonald ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Blood Gases ◽  
Catostomus Commersoni ◽  
Acid Base ◽  
Aortic Blood ◽  
Respiratory Parameters ◽  
Arterial Ph ◽  
O2 Extraction ◽  
Acid Base Status ◽  
Aortic Blood Pressure

Blood gases, acid-base status, plasma ions, respiration, ventilation and cardiovascular function were measured in white suckers, using standard cannulation methods. Basic respiratory parameters under normoxia were compared to those in the active, pelagic rainbow trout and in other benthic teleosts. Sustained environmental hyperoxia (350–550 torr) increased arterial O2 (102–392 torr) and venous O2 (17–80 torr) tensions so that blood O2 transport occurred entirely via physical solution. Dorsal aortic blood pressure and heart rate fell, the latter due to an increase in vagal tone. Ventilation volume declined markedly (by 50%) due to a decrease in ventilatory stroke volume, but absolute O2 extraction rose so that O2 consumption was unaffected. While the preceding effects were stable with time, arterial and venous CO2 tensions approximately doubled within 4 h, and continued to increase gradually thereafter. This CO2 retention caused an acidosis (7.993–7.814) which was gradually compensated by an accumulation of plasma [HCO3−]. However, even after 72 h, arterial pH remained significantly depressed by 0.10 units. The gradual rise in plasma [HCO3−] was accompanied by a progressive fall in both [Na+] and [Cl−]; [K+] and [Ca2+] remained unchanged. The responses of the sucker to hyperoxia are compared to those of the rainbow trout.

Acid-Base Effects of Combined Renal Deletion of NBCe1-A and NBCe1-B

2022 ◽  
Author(s):  
Hyun-Wook Lee ◽  
Jill W. Verlander ◽  
Gary E Shull ◽  
Autumn N. Harris ◽  
I. David Weiner
Keyword(s):  
Proximal Tubule ◽  
Splice Variant ◽  
Molecular Mechanisms ◽  
Ammonia Excretion ◽  
Basal Diet ◽  
Acid Base ◽  
Outer Medulla ◽  
Ammonia Metabolism ◽  
Induced Changes ◽  
Acid Loading

The molecular mechanisms regulating ammonia metabolism are fundamental to acid-base homeostasis. Deleting the A splice variant of the Na⁺-bicarbonate cotransporter, electrogenic, isoform 1 (NBCe1-A) partially blocks the effect of acidosis to increase urinary ammonia excretion, and this appears to involve the dysregulated expression of ammoniagenic enzymes in the proximal tubule (PT) in the cortex, but not in the outer medulla (OM). A second NBCe1 splice variant, NBCe1-B, is present throughout the PT, including the OM, where NBCe1-A is not present. The current studies determined the effects of combined renal deletion of NBCe1-A and NBCe1-B on systemic and proximal tubule ammonia metabolism. We generated NBCe1-A/B deletion using Cre-loxP techniques and used Cre-negative mice as controls. Since renal NBCe1-A and NBCe1-B expression is limited to the proximal tubule, Cre-positive mice had proximal tubule NBCe1-A/B deletion (PT-NBCe1-A/B KO). While on basal diet, PT-NBCe1-A/B KO mice had severe metabolic acidosis, yet urinary ammonia excretion was not changed significantly. PT-NBCe1-A/B KO decreased expression of phosphate-dependent glutaminase (PDG) and phospho­enol­pyruvate carboxy­kinase (PEPCK) and increased expression of glutamine synthetase (GS), an ammonia recycling enzyme, in PT in both the cortex and OM. Exogenous acid-loading increased ammonia excretion in control mice, but PT-NBCe1-A/B KO prevented any increase. PT-NBCe1-A/B KO significantly blunted acid loading-induced changes in PDG, PEPCK, and GS expression in the proximal tubule in both the cortex and OM. We conclude that NBCe1-B, at least in the presence of NBCe1-A deletion, contributes to proximal tubule ammonia metabolism in the OM and thereby to systemic acid-base regulation.

scholarly journals KIDNEY AND URINARY BLADDER RESPONSES OF FRESHWATER RAINBOW TROUT TO ISOSMOTIC NaCl AND NaHCO3 INFUSION

1992 ◽  
Vol 173 (1) ◽  
pp. 181-203 ◽  
Author(s):  
B. James-Curtis ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Urinary Bladder ◽  
Metabolic Alkalosis ◽  
Bladder Function ◽  
Acid Base ◽  
Burst Frequency ◽  
Arterial Ph ◽  
Acid Base Status ◽  
Nacl Load ◽  
Kidney Functions

The relative roles of the kidney and urinary bladder in ion, fluid and acid-base regulation were examined in freshwater rainbow trout chronically infused with either 140 mmol l-1 NaCl or 140 mmol l-1 NaHCO3 (3 ml kg-1 h-1) for 32 h. NaCl had a negligible effect on blood ionic and acid-base status, whereas NaHCO3 induced a metabolic alkalosis characterized by a rise in arterial pH and [HCO3-] and an equimolar fall in [Cl-]. Urine was collected via either an internal catheter, which bypassed bladder function, or an external urinary catheter, which collected naturally voided urine. As a percentage of the infusion rate, glomerular filtration rate increased by about 135 %, but urine flow rate (UFR) by only 80 %, reflecting increased tubular reabsorption of H2O. During NaCl infusion, virtually all of the extra Na+ and Cl- filtered was reabsorbed by the kidney tubules, resulting in an increased UFR with largely unchanged composition. During NaHCO3 infusion, tubular Na+ and Cl- reabsorption again kept pace with filtration. HCO3- reabsorption also increased, but did not keep pace with filtration; an increased flow of HCO3--rich urine resulted, which excreted about 10 % of the infused base load. At rest, fish fitted with external catheters voided in discrete bursts of about 0.85 ml kg-1 at 25 min intervals. During infusion, burst frequency increased by about 40 % and burst volume by about 20 %. Reabsorption by the bladder reduced UFR by 25 %, the excretion of Na+ and Cl- by 50 %, of K+ by 44 % and of urea by 25 %. These differences persisted on a relative basis during NaCl and NaHCO3 infusion despite the decreased residence time. However, HCO3- was neither secreted nor reabsorbed by the bladder. We conclude that the freshwater kidney functions to remove as much NaCl as possible from the urine, regardless of the NaCl load, and this role is supplemented by bladder function. The bladder plays no role in acid-base regulation during metabolic alkalosis.

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