Hormone‐induced co‐transport with specific pharmacological properties in erythrocytes of rainbow trout, Salmo gairdneri.

Baroin, Anne; Garcia-Romeu, F; Lamarre, T; Motais, R

doi:10.1113/jphysiol.1984.sp015193

Cited by 50 publications

(33 citation statements)

References 34 publications

(38 reference statements)

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“…We also believe that such a shift was responsible (in part) for the increased pcv and serum proteins in BGD-infected trout. Other factors, not directly related to ion dilution, may also have contributed to the haemoconcentration including, for example, stress-and/or hypoxemicinduced release of catecholamines which cause swelling of erythrocytes, thus increasing the pcv (Nikinmaa 1982, Baroin et al 1984, Motais et al 1989. The mechanism(s) for ion dilution in these fish may be quite unlike those of trout with BGD, but the sequelae and eventual outcome may nevertheless be similar.…”

Section: Discussionmentioning

confidence: 99%

Blood chemistry of bacterial gill disease in brook trout Salvelinus fontinalis

Byrne¹,

Ferguson²,

Lumsden³

et al. 1991

Dis. Aquat. Org.

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Blood chemistry was examined in brook trout Salvelinus fontinalis suffering from bacterial gdl disease (BGD) and compared to normal healthy fish under identical conditions. Infected fish showed a marked decrease in serum Na+, Cl-and in osmolality, and a concommitant haemoconcentration as indicated by the increased serum protein and increased packed cell volume. Fish with BGD exhibited an mcreased rate of respiration (tachybranchia) but were not hypoxemic, suggesting that compensatory mechanisms, such as tachybranchia and enhanced recruitment of lamellar reserves, were successful. Nevertheless, the cause of the tachybranchia in BGD-infected fish remains unexplained; it may not be a response to impaired oxygen exchange, although this seems the most likely explanation. The acid-base status did not differ between healthy and diseased fish. These findings suggest that changes in blood components other than acid-base ones constitute the critical, and sometimes fatal changes occurring as a result of BGD infection, rather than hypoxemia. It is suggested that circulatory disturbances resulted from the rapid drop of blood electrolytes, which in turn triggered a fluid shift from the extracellular to the intracellular compartments, leading to haemoconcentration and death. However caused, tachybranchia probably exacerbated the worsening blood chemistry changes resulting from damaged gill epithelium. The implications of these findings for treatment include reducing the rate of ion loss from the gills by raising the salt levels in the water, combined with other chemicals directed specifically at the bacteria.

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Section: Discussionmentioning

confidence: 99%

Blood chemistry of bacterial gill disease in brook trout Salvelinus fontinalis

Byrne¹,

Ferguson²,

Lumsden³

et al. 1991

Dis. Aquat. Org.

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“…Since NaCl co-transport has been found and described in the presence of CO2 (Baroin et al 1984), an increase in intracellular pH cannot be requisite for the induction of the NaCl co-transport. Experiments determining the relationship between Na+-H+ exchanger and NaCl co-transport are in progress.…”

Section: Na+-h+ Exchanges Induced By Catecholaminesmentioning

confidence: 99%

“…This increase in volume is the result of net uptake of Na+ and osmotically obligated water (Baroin, Garcia-Romeu, Lamarre & Motais, 1984). Two different pathways are involved in the salt uptake.…”

Section: Introductionmentioning

confidence: 99%

A transient sodium‐hydrogen exchange system induced by catecholamines in erythrocytes of rainbow trout, Salmo gairdneri.

Baroin¹,

Garcia-Romeu²,

Lamarre³

et al. 1984

The Journal of Physiology

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119

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SUMMARY1. The addition of isoprenaline to an isotonic suspension of red blood cells of rainbow trout induces an amiloride-sensitive Na+ transport which is independent of Cl-and insensitive to 4,4'-diisothiocyano-2,2'-stilbene disulphonic acid (DIDS) and furosemide.2. Na+ uptake is accompanied by amiloride-sensitive H+ release. The H+ efflux is dependent upon the external Na+ concentration, the Ko.5 value for Na+ being 16 mm.3. In the presence of DIDS, when the coupled NaCl entry (NaCl co-transport) induced by catecholamine is blocked, the results provide evidence for a linked movement of Na+ and H+, with a stoicheiometry of 1 :1.4. Exchange of H+ for Na+ induces osmotic swelling of the cells which is due to the replacement of a bound proton by an osmotically active Na+ cation.5. In the absence of DIDS when the bulk of the Na+ uptake is the result of a coupled entry of Na+ and Cl-, H+ extrusion still occurs and the magnitude of acid excretion is identical to that found in DIDS-treated cells. This suggests that Na+-H+ exchange remains active.6. Addition of isoprenaline first stimulates the Na+-H+ exchange but only transiently. This is followed by a more permanent stimulation ofthe NaCl co-transport.

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“…Measurements were made as previously described (Baroin et al 1984a). A trapping correction of 1-5% was routinely applied to the final calculation (Borgese et al 1986).…”

Section: Experimental Solutionsmentioning

confidence: 99%

“…Thus the basic pattern of cell enlargement is similar in avian and trout red cells, but the response is achieved by different transport mechanisms. In avian red cells the net Na+ gain occurs through a furosemide-bumetanide-sensitive Na+ + K+ + 2Cl-co-transport, whereas in trout erythrocytes NaCl uptake is K+ independent and sensitive to inhibition by amiloride and 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS) (Baroin et al 1984a). The strong acidification of the medium which occurs at the onset of stimulation has been explained by the fact that part of the Na+ that penetrates the cell is exchanged with H+, which comes from the intracellular buffer, via a Na+-H+ exchange mechanism with a stocheiometry of 1: 1 (Baroin et al 1984b; Cossins & Richardson, 1985).…”

mentioning

confidence: 99%

Control of cell volume and ion transport by beta‐adrenergic catecholamines in erythrocytes of rainbow trout, Salmo gairdneri.

Borgèse¹,

Garcia-Romeu²,

Motais³

1987

The Journal of Physiology

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SUMMARY1. Trout red cells suspended in an isotonic medium containing fl-adrenergic catecholamines or adenosine 3',5'-phosphate (cyclic AMP) enlarge rapidly to reach a new steady-state volume which is maintained as long as hormone is present. The volume response is not changed by inhibition of the Na+-K+ pump with ouabain. The new steady-state volume was shown to result from a dynamic equilibrium involving the simultaneous functioning of two regulatory processes induced by hormone: a volume increase response that causes cells to enlarge by gaining Na+ and a volume decrease response that causes cells to shrink by losing K+.2. As previously described, the volume increase response due to NaCl entry, is mediated by the activation by cyclic AMP of a Na+-H+ antiport operating in parallel to Cl--OH-exchanges. In addition, it is shown in this paper that the Na+ uptake is a discontinuous, oscillatory process and that NaCl entry continues for several hours, i.e. as long as hormone is present.3. The volume decrease response involves a passive, Cl--dependent K+ loss. Na+ cannot use this pathway. The response is blocked by replacement of Cl-by NO3-, by loop diuretics (furosemide, bumetanide) but also by inhibitors of the anion exchanger (4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS), niflumic acid). The activation of this ouabain-insensitive, Cl--dependent K+ transport system is not directly triggered by cyclic AMP. It involves an all-or-none type of switching phenomenon which occurs when the cells swell to a certain volume. Thus it is a regulatory response to the increase in cell volume induced by stimulation of the Na+-H+ exchange by cyclic AMP. Inactivation is also volume dependent: when the cell size approaches the initial size the pathway shuts off. Thus the controlling mechanism of the K+ pathway acts like a reversible on-off switch that operates around a given volume. Ca2+ was not found to be involved in this control. Cyclic AMP is not necessary to keep the activated K+ pathway open but it could be one of the factors involved in the activating process.4. There are several lines of evidence indicating that in trout red cells the volume decrease and the volume increase responses may not be brought about by the same

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Hormone‐induced co‐transport with specific pharmacological properties in erythrocytes of rainbow trout, Salmo gairdneri.

Cited by 50 publications

References 34 publications

Blood chemistry of bacterial gill disease in brook trout Salvelinus fontinalis

Blood chemistry of bacterial gill disease in brook trout Salvelinus fontinalis

A transient sodium‐hydrogen exchange system induced by catecholamines in erythrocytes of rainbow trout, Salmo gairdneri.

Control of cell volume and ion transport by beta‐adrenergic catecholamines in erythrocytes of rainbow trout, Salmo gairdneri.

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