Acid-Base and Ionic Exchanges at Gills and Kidney After Exhaustive Exercise in the Rainbow Trout

1988 ◽  
Vol 136 (1) ◽  
pp. 461-481 ◽  
Author(s):  
CHRIS M. WOOD

Unidirectional Na+ and Cl− fluxes, net fluxes of Na+, Cl−, other ions, titratable acid (TA), ammonia and acidic equivalents (net H+) across the gills, together with the comparable renal fluxes, were monitored throughout a 24-h period after exhaustive exercise (simple chasing) in the rainbow trout. The gills were the major site of flux. The renal excretion of [TA-HCO3−], ammonia, lactate and most electrolytes increased after exercise, coincident with diuresis. Relative to the gills, the kidney accounted for only 8% of net H+ flux, 0–15% of net electrolyte losses and 50% of lactate loss, though the latter was negligibly small. Approximately 1000 μequiv kg−1 of net H+ were transported across the gills to the water during the first 4h, and then fully recovered over the subsequent 8h, coincident with periods of extracellular acidosis and alkalosis recorded in previous studies. Ammonia efflux increased during the first 4h; changes in titratable acid flux and extracellular PNHNH3 and NH4+ levels suggest that this elevation occurred partially as NH3 diffusion in the first hour, and thereafter mainly as NH4+ exchange. Small net Na+ losses (≊300 μequivkg−1), moderate net K+ losses (≊600 μequiv kg−1) and large net Cl− losses (≊1200 μequiv kg−1) correlated well with previously reported plasma changes; only the Na+ deficit was fully corrected by 24 h. Na+ influx was stimulated and Cl− influx inhibited during the 0–4 h period of net H+ excretion, whereas Na+ influx returned to control levels and Cl− influx increased during the 4–12 h period of net H+ uptake. These data indicate dynamic modulation of Na+/NH4+,H+ and C1−/HCO3−,OH− exchanges; however, an excess of Cl− over Na+ efflux also contributed to net H+ excretion. Acidic equivalent flux correlated well with [Na+-Cl−] net flux, in accord with strong ion difference theory.

1989 ◽  
Vol 147 (1) ◽  
pp. 471-491 ◽  
Author(s):  
D. G. MCDONALD ◽  
Y. TANG ◽  
R. G. BOUTILIER

Rainbow trout, fitted with arterial catheters, were exercised to exhaustion by manual chasing and then injected with either saline (controls), the β-agonist isoproterenol or the β-antagonist propranolol. Blood acid-base status, branchial unidirectional and net fluxes of Na+ and Cl−, and net fluxes of ammonia and acidic equivalents (JHnet) were monitored over the subsequent 4 h of recovery. These same parameters were also monitored in normoxic, resting fish following isoproterenol injection and in exercised fish following acute post-exercise elevation of external NaCl concentration. In addition to confirming an important role for β-adrenoreceptors in the regulation of branchial gas exchange and red cell oxygenation and acid-base status, we find a significant β-adrenergic involvement in the flux of lactic acid from muscle and in JHnet across the gills. Both isoproterenol infusion (into nonexercised fish) and exhaustive exercise were found to cause net acid excretion. The post-exercise JHnet was further augmented by elevating [NaCl] but was not affected, in this instance, either by β-stimulation or blockade, indicating that JHnet was not entirely regulated by a β-adrenergic mechanism. On the basis of a detailed analysis of unidirectional Na+ and Cl− fluxes, we conclude that the increase in JHnet following exercise arose mainly from increased Na+/H+(NH4+) exchange and that the upper limit on JHnet was set by the supply of external counterions and by the increase in branchial ionic permeability that invariably accompanies exhaustive exercise.


1990 ◽  
Vol 152 (1) ◽  
pp. 521-547 ◽  
Author(s):  
GREG G. GOSS ◽  
CHRIS M. WOOD

Endogenous respiratory acidosis and metabolic alkalosis were induced in bladder-catheterized freshwater rainbow trout by exposure to environmental hyperoxia (72 h) and its subsequent removal. Unidirectional and net fluxes of Na+, Cl− and acidic equivalents across the gills were examined over 0.5 h intervals. Hyperoxia resulted in a positive Na+ balance, negative Cl− balance and net acidic equivalent excretion. Return to normoxia caused a negative Na+ balance, a positive Cl− balance and net basic equivalent excretion (=acidic equivalent uptake). Cl−/basic equivalent exchange was more important than Na+/acidic equivalent exchange in the homeostatic responses, and alkalosis was a more potent stimulus than acidosis for change in branchial ion fluxes. Kinetic analysis demonstrated that alterations in ion fluxes were achieved by complex changes in both the Km (inverse of affinity) and the Jmax (maximal transport rate) of the branchial Cl−/HCO3−(OH−) and Na+/H+(NH4+) transporters. KmCl (control=165 μequiv l−1) and KmNa (114 μequiv l−1) were increased during hyperoxic acidosis to 250 and 445 μequiv l−1, respectively. JmaxCl, (291 μequiv kg−1 h−1) and JmaxNa (456 μequiv kg−1 h−1) did not change significantly. During post-hyperoxic alkalosis, KmNa was further increased to 559 μequiv l−1, JmaxCl increased to 445 μequiv kg−1 h−1, while KmCl and JmaxNa decreased to 137 μequiv l−1 and 309 μequiv kg−1 h−1, respectively. Diffusive efflux was examined using a novel method. There was no significant differential diffusive efflux of Na+ and Cl− during hyperoxia but diffusive Na+ efflux exceeded Cl− efflux during posthyperoxic alkalosis, thereby serving as an additional mechanism for basic equivalent excretion.


1987 ◽  
Vol 128 (1) ◽  
pp. 255-267 ◽  
Author(s):  
M. G. Vermette ◽  
S. F. Perry

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.


1974 ◽  
Vol 60 (3) ◽  
pp. 769-781
Author(s):  
T. J. SHUTTLEWORTH ◽  
R. F. H. FREEMAN

1. Measurements of net flux of water have been made on isolated gills removed from freshwater-adapted and seawater-adapted eels and incubated in various media of differing osmotic pressure. 2. From these measurements it has been possible to determine the osmotic permeability coefficient of the gill directly from the net water flux. The values obtained (0.50±0.14x10-5 cm.sec-1 for freshwater eels and 0.43±0.07x10-5 cm.sec-1 for seawater-adapted eels) indicate that there was no significant change in this parameter on adaptation of the eels to sea water. 3. The direct measurements made of the net water flux across the isolated gills appear to be compatible with the osmoregulatory pattern of eels as deduced by other workers using different techniques. In particular they illustrate and further emphasize the significance of drinking in the freshwater fish. 4. Calculations indicate that, for a freshwater teleost, the osmotic and ionic problems caused by drinking in fresh water have an insignificant energetic effect and hence, energetically, it matters little to the fish whether it drinks or not.


1991 ◽  
Vol 156 (1) ◽  
pp. 153-171 ◽  
Author(s):  
YONG TANG ◽  
ROBERT G. BOUTILIER

The intracellular acid-base status of white muscle of freshwater (FW) and seawater (SW) -adapted rainbow trout was examined before and after exhaustive exercise. Exhaustive exercise resulted in a pronounced intracellular acidosis with a greater pH drop in SW (0.82 pH units) than in FW (0.66 pH units) trout; this was accompanied by a marked rise in intracellular lactate levels, with more pronounced increases occurring in SW (54.4 mmoll−1) than in FW (45.7 mmoll−1) trout. Despite the more severe acidosis, recovery was faster in the SW animals, as indicated by a more rapid clearance of metabolic H+ and lactate loads. Compartmental analysis of the distribution of metabolic H+ and lactate loads showed that the more rapid recovery of pH in SW trout could be due to (1) their greater facility for excreting H+ equivalents to the environmental water [e.g. 15.5 % (SW) vs 5.0 % (FW) of the initial H+ load was stored in external water at 250 min post-exercise] and, to a greater extent, (2) the more rapid removal of H+, facilitated via lactate metabolism in situ (white muscle) and/or the Cori cycle (e.g. heart, liver). The slower pH recovery in FW trout may also be due in part to greater production of an ‘unmeasured acid’ [maximum approx. 8.5 mmol kg−1 fish (FW) vs approx. 6 mmol kg−1 fish (SW) at 70–130 min post-exercise] during the recovery period. Furthermore, the analysis revealed that H+-consuming metabolism is quantitatively the most important mechanism for the correction of an endogenously originating acidosis, and that extracellular pH normalization gains priority over intracellular pH regulation during recovery of acid-base status following exhaustive exercise.


1989 ◽  
Vol 141 (1) ◽  
pp. 407-418 ◽  
Author(s):  
Y. TANG ◽  
D. G. McDONALD ◽  
R. G. BOUTILIER

Blood acid-base regulation following exhaustive exercise was investigated in freshwater- (FW) and seawater- (SW) adapted rainbow trout (Salmo gairdneri) of the same genetic stock. Following exhaustive exercise at 10°C, both FW and SW trout displayed a mixed respiratory and metabolic blood acidosis. However, in FW trout the acidosis was about double that of SW trout and arterial blood pH took twice as long to correct. These SW/FW differences were related to the relative amounts of net H+ equivalent excretion to the environmental water, SW trout excreting five times as much as FW trout. The greater H+ equivalent excretion in SW trout may be secondary to changes in the gills that accompany the adaptation from FW to SW. It may also be related to the higher concentrations of HCO3− as well as other exchangeable counter-ions (Na+ and Cl−) in the external medium in SW compared to FW.


1967 ◽  
Vol 50 (6) ◽  
pp. 1607-1625 ◽  
Author(s):  
J. A. Raven

The concentrations of K, Na, and Cl in the cytoplasm and vacuole, the tracer fluxes of these ions into and out of the cenocyte, and the electrical potential difference between bathing solution and vacuole and cytoplasm, have been measured in Hydrodictyon africanum. If the ions were acted on solely by passive electrochemical forces, a net efflux of K and Cl and a net influx of Na would be expected. Tracer fluxes indicate a net influx of K and Cl and efflux of Na in the light; these net fluxes are consequently active, with an obligate link to metabolism. The effects of darkness and low temperature indicate that most of the tracer K and Cl influx and Na efflux are linked to metabolism, while the corresponding tracer fluxes in the direction of the free energy gradient are not. Ouabain specifically inhibits the metabolically linked portions of tracer K influx and Na efflux. Alterations in the external K concentration have similar effects on metabolically mediated K influx and Na efflux. It would appear that K influx and Na efflux are linked, at least in the light.


1986 ◽  
Vol 250 (5) ◽  
pp. F781-F784 ◽  
Author(s):  
S. Tsuboi ◽  
R. Manabe ◽  
S. Iizuka

Transport of Na and Cl across the isolated dog retinal pigment epithelium (RPE) choroid was investigated. Under the short-circuit condition, a net Na flux was observed from choroid to retina and a net Cl flux was determined in the opposite direction. The current created by the net flux of these two ions was larger than the short-circuit current (SCC). Addition of 10(-5) M ouabain to the apical side inhibited net fluxes of both Na and Cl, whereas it reduced the SCC 84%. Addition of 10(-4) M furosemide to the apical side inhibited net Cl flux but had no effect on the net Na transport. The 10(-4) M furosemide reduced the SCC 38%. These drugs had no effect when applied to the basal side. Thus the transport of both Na and Cl depends on the Na-K-ATPase in the apical membrane of the dog RPE. A furosemide-sensitive neutral carrier at the apical membrane is suggested for the transport of Cl. Replacement of HCO3 with SO4 in the bathing solution caused an increase in the SCC, indicating the choroid-to-retina movement of HCO3 across the short-circuited dog RPE choroid.


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