Cell volume regulation by trout erythrocytes: characteristics of the transport systems activated by hypotonic swelling.

Garcia-Romeu, F; Cossins, Andrew R.; Motais, R

doi:10.1113/jphysiol.1991.sp018724

Cited by 101 publications

(68 citation statements)

References 32 publications

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“…In addition, the volume-activated K+ pathway in this case is essentially Cl-independent, i.e. K+ loss is not, or only slightly, reduced by replacement of Cl-by NO3- (Garcia-Romeu, Cossins & Motais, 1991). Thus in trout erythrocytes two types of volume-dependent K+ pathways co-exist, and we have demonstrated that the cells adopt one rather than the other depending on changes of cellular ionic strength induced by swelling (Motais, Guizouarn & Garcia-Romeu, 1991).…”

Section: Introductionmentioning

confidence: 59%

Volume‐activated Cl(‐)‐independent and Cl(‐)‐dependent K+ pathways in trout red blood cells.

Guizouarn

Harvey

Borgèse

et al. 1993

The Journal of Physiology

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SUMMARY1. Swelling of trout erythrocytes can be induced either by addition of catecholamine to the cell suspension, thus promoting NaCl uptake via fiadrenergic-stimulated Na+-H+ exchange (isotonic swelling) or by suspending red blood cells in a hypotonic medium (hypotonic swelling). In both cases cells tend to regulate their volume by losing K+, but the characteristics of the volume-activated K+ pathways are different: after hormonally induced swelling the K+ loss is strictly Cl-dependent; after hypotonic swelling the K+ loss is essentially Cl-independent.2. In order to determine the nature of these volume regulatory pathways (i.e. whether the net K+ loss was conductive or was by electroneutral K+-H+ exchange or KCl co-transport), studies were performed to analyse ion fluxes and associated electrical phenomena. The cell membrane potential and intracellular ionic activities of volume-regulating and volume-static cells were measured by impalement with conventional microelectrodes and double-barrelled ion-sensitive microelectrodes.3. The information gained from the electrical and ion flux studies leads to the conclusion that both Cl--independent and Cl--dependent K+ loss proceed via electrically silent pathways.4. Experiments were designed to distinguish between electroneutral K+-H+ exchange or KCI co-transport. These were based upon the inhibition of Cl--OHexchange to evaluate the degree of coupling between K+ and Cl-(KCI stoichiometry, pH change). The experimental observations are consistent with the fact that both Cl--independent and Cl--dependent K+ loss are mediated by coupled K+-anion co-transport and not by K+-H+ exchange.5. On the basis of previous data, we suggest that only one type of K+-anion cotransport exists in the cell membrane, for which the selectivity for anions varies according to the change in cellular ionic strength induced by swelling.

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Section: Introductionmentioning

confidence: 59%

Volume‐activated Cl(‐)‐independent and Cl(‐)‐dependent K+ pathways in trout red blood cells.

Guizouarn

Harvey

Borgèse

et al. 1993

The Journal of Physiology

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“…As shown in fish erythrocytes in particular (Garcia-Romeu et al 1991;Goldstein & Brill, 1991;Kirk et al 1992;Haynes & Goldstein, 1993), this volume-activated efflux is inhibited by inhibitors of anion exchangers (DIDS and niflumic acid), and of chloride channels (NPPB,MK 196), but not by inhibitors of Na+-K+-2Cl-cotransport (frusemide). It has been proposed that the volume-stimulated taurine efflux behaves more like a chloride channel than a saturable carrier.…”

Section: Discussionmentioning

confidence: 99%

“…This contribution has been described in invertebrates and also in mammalian tissues such as cardiac cells (Thurston, Hauhart & Naccarato, 1981), Ehrlich cells (Hoffmann & Lambert, 1983;Lambert, 1984;Lambert & Hoffmannn, 1993) (Fugelli & Thoroed, 1986;Kirk, Ellory & Young, 1992), the skate (Goldstein & Brill, 1990, the eel (Fincham, Wolowyk & Young, 1987) and the trout (Garcia-Romeu, Cossins & Motais, 1991), and also in the cyclostomes, hagfish and lamprey (Brill, Musch & Goldstein, 1992).…”

Section: Introductionmentioning

confidence: 99%

Effects of hyposmotic shock on taurine transport in isolated trout hepatocytes

Michel¹,

Fossat²,

Porthé-Nibelle³

et al. 1994

Experimental Physiology

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SUMMARYIsolated trout hepatocytes exposed to hypotonic medium undergo a regulatory volume decrease (RVD) that occurs via two separate routes, K+-Cl-cotransport and amino acid release, the ion efflux accounting for 70 % of the total osmolyte loss. Taurine, glutamine and glutamic acid are the most important and represent 73 % of the total amino acid content (53 mmol (1 cell water)-').The osmolarity-sensitive release of amino acids was studied using [3H]taurine. Kinetic studies indicated two components for taurine influx: a linear Na+-independent transport and a saturable Na+-dependent system with a Michaelis-Menten constant (K.) of 122 fSM and a maximum velocity (Vmax) of 31-2 pmol (mg protein)-1 min-'. This second way of uptake was also chloride dependent and indicated an apparent coupling ratio Na+: Cl-: taurine of 2:1:1. The latter component and the taurine efflux were stimulated during RVD, leading to intracellular amino acid loss. Taurine efflux activation during volume recovery was transient and also dependent on the presence of both Na+ and Cl-in the extracellular medium. Furthernore, taurine release and RVD were slowed down when Ca2l was omitted from the medium. These results suggested two distinct and complementary mechanisms for volume regulation in trout hepatocytes during hypotonic conditions.

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“…By expression studies of tAE1 in Xenopus oocytes, we have demonstrated previously that this normally electroneutral anion exchanger is able to form an anion conductive path-way permeable to different charged or neutral osmolytes such as urea, choline, sorbitol, Na ϩ , and K ϩ (13)(14)(15). In physiological conditions, these transport properties of tAE1 are activated by a decrease in intracellular ionic strength in swollen erythrocytes, and they are involved in the cell regulatory volume decrease response (16,17). Here, we focused on another unexpected feature of this anion exchanger.…”

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confidence: 99%

Evidence for Up-regulation of the Endogenous Na-K-2Cl Co-transporter by Molecular Interactions with the Anion Exchanger tAE1 Expressed in Xenopus Oocyte

Guizouarn

Gabillat

Borgèse

2004

Journal of Biological Chemistry

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Expression of trout anion exchanger 1 (tAE1) in Xenopus oocyte led to the stimulation of a Na ؉ -and Cl ؊ -dependent Rb influx. Functional features and pharmacological data strongly suggest that this Rb influx is mediated by the endogenous Na-K-2Cl (NKCC) co-transporter. The functional relationship between expression of tAE1 and activation of the NKCC co-transporter was investigated. Indeed, it was shown previously that tAE1 expressed in Xenopus oocyte induces a strong anion conductance which is correlated with an increased taurine permeability. Measurements of intracellular ion contents ruled out the involvement of any modification of known electrochemical parameters in NKCC co-transporter activation by tAE1. Furthermore, using chimera of tAE1 made with AE1 from other species unable to exhibit anion conductance led to the conclusion that there was no correlation between tAE1 anion conductance and NKCC co-transporter stimulation. Therefore, a possible molecular interaction between tAE1 and the NKCC co-transporter was investigated. Our results clearly show that NKCC activation is dependent upon the C-terminal part of tAE1. Chimeric constructions where tAE1 C-terminal part was substituted by the corresponding part of mouse AE1 abolished co-transporter activation. Moreover, steric encumbrance on the C-terminal end of tAE1 with a specific antibody or with a protein fusion also prevented the co-transporter activation. These data suggest a new role for some anion exchangers in controlling other transporter activity by molecular interactions.

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Cell volume regulation by trout erythrocytes: characteristics of the transport systems activated by hypotonic swelling.

Cited by 101 publications

References 32 publications

Volume‐activated Cl(‐)‐independent and Cl(‐)‐dependent K+ pathways in trout red blood cells.

Volume‐activated Cl(‐)‐independent and Cl(‐)‐dependent K+ pathways in trout red blood cells.

Effects of hyposmotic shock on taurine transport in isolated trout hepatocytes

Evidence for Up-regulation of the Endogenous Na-K-2Cl Co-transporter by Molecular Interactions with the Anion Exchanger tAE1 Expressed in Xenopus Oocyte

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