Volume-responsive sodium and proton movements in dog red blood cells.

Jc, Parker; Castranova,

doi:10.1085/jgp.84.3.379

Cited by 82 publications

(40 citation statements)

References 23 publications

(71 reference statements)

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“…In spite of the fact that NaCl uptake is practically independent of the presence of HCO3-in the external medium and swelling is largely inhibited when Cl-is replaced by N03-, it was suggested that the catecholamine-induced volume increase is mediated by the activation of a Na+-H+ antiport which operates in parallel to a Cl--OH-exchanger, rather than by a NaCl co-transport (Borgese, Garcia-Romeu & Motais, 1986). It should be noted that other systems such as Amphiuma and dog erythrocytes and human blood lymphocytes regulate their volume in response to osmotic shrinkage by the stimulation of a Na+-H+ antiport operating in parallel to a Cl--HC13-exchanger (Cala, 1980(Cala, , 1983bParker, 1983b;Parker & Castranova, 1984;Grinstein, Clarke & Rothstein, 1983;Kregenow, Caryk & Siebens, 1985). These responses do not involve cyclic AMP, however.…”

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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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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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“…In epithelial (Spring and Ericson, 1982) and blood cells (Cala, 1983;Parker and Castranova, 1984;Grinstein et al, 1985b), as well as in Ehrlich ascites cells (Hoffmann, 1985), a regulatory volume increase is observed in response to anisotonic shrinking. Swelling in these cases is thought to be osmotic, due to uptake of solutes and associated water.…”

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confidence: 99%

Volume changes in activated human neutrophils: The role of Na⁺/H⁺ exchange

Grinstein

Furuya

Cragoe

1986

Journal Cellular Physiology

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The apparent volume of neutrophils, as measured electronically with the Coulter counter, has been reported to increase upon treatment with chemotactic factors. The occurrence of a volume change was confirmed by forward angle light scattering and by isotopic measurements of intracellular water space in cells treated with 12-O-tetradecanoylphorbol 13,acetate (TPA) or formyl-methionyl-leucyl-phenylalanine (FMLP). Cell swelling was associated with an increase in the osmotic content of the cells, determined from Boyle-van't Hoff plots, and with an increase in Na+ content, measured by flame photometry. The volume change was inhibited by replacement of extracellular Na+ with K+ or N-methyl-D-glucamine+, or by addition of amiloride. Swelling was also inhibited by the 5-N-substituted analogs of amiloride, which are potent specific inhibitors of the Na+/H+ antiport. This pathway is activated in neutrophils by both TPA and FMLP. Activation of Na+/H+ exchange, determined as a Na+ -dependent and amiloride-sensitive cytoplasmic alkalinization, was also found when neutrophils were treated with hypertonic solutions. The hypertonic activation of the antiport was similarly followed by cell swelling, detectable by electronic sizing. The results indicate that activation of Na+/H+ exchange can lead to significant cell swelling in neutrophils.

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“…the intracellular pH would be expected to have decreased to below 7.0 in the previous study [10]. The 'set point' of the Na+/H+ exchanger in Ehrlich cells is 7.0 [31] and the Na+ uptake seen at pH0 7.0 might, therefore, be attributed mainly to an activation of Na+/H+ exchange, which in some systems is anion-sensitive [33], rather than Na+-dependent anion exchange. This is also supported by the observation that net Na+ influx was lower at pH0 7.0 than at 7.4, in agreement with the observation that pH re covery by Na+/H + exchange is slower and less complete than by Na+-dependent anion ex change [23].…”

Section: Discussionmentioning

confidence: 74%

HgCI<sub>2</sub>-lnduced Ion Transport Pathways in Ehrlich Ascites Tumor Cells

Jensen

Kramhøft²,

Jessen³

et al. 1993

Cell Physiol Biochem

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HgCl₂ (40 µM) initially activates an anion-independent unidirectional Na⁺ influx in Ehrlich ascites tumor cells, which amounts to 61 ± 7 µmol·g dry wt^-1 min^-1 (± SEM, n = 5). The unidirectional Na⁺ influx in control cells in 13 ± 2 µmol·dry wt^-1 • min^-1 (± SEM, n = 5). The HgCl₂-activated Na⁺ influx is slightly inhibited by amiloride (inhibitor of Na⁺/H⁺ exchange), but almost completely blocked by the anion-exchange inhibitor DIDS (4,4’-diisothiocyano-2,2’-stilbenedisulfonic acid). HgCl₂ also causes DIDS-sensitive cytoplasmic acidification followed by DIDS-sensitive cytoplasmic alkalinization. After addition of HgCl₂ the cells initially shrink, whereupon they swell again. Half-maximal effect of HgCl₂ is obtained with about 0.5 and 1 µM HgCl₂ on cell swelling and cell shrinkage, respectively. The volume responses are both reduced in the presence of DIDS. The unidirectional K⁺ and Cl^– effluxes are greatly stimulated by HgCl₂. The stimulation of K⁺ efflux results in a Cl^--dependent net loss of K⁺. In Cl^– medium the K⁺ loss is 84 ± 11 µmol·g dry wt^–1 • min^–1 ( ± SEM, n = 6). In NO^–₃ medium, it is reduced to 24 ± 6 µmol·g dry wt^-1 • min^-1 ( ± SEM, n = 4). The HgCl₂ activated K⁺ efflux in Cl^– medium is reduced to 21 ± 6 µmol·g dry wt^–1 • min^–1 ( ± SEM, n = 3) by DIDS. Finally, an instantaneous hyperpolarization of the cell membrane potential was observed after addition of HgCl₂. It is concluded that HgCl₂ in Ehrlich cells activates (i) a DIDS-sensitive, Na⁺-dependent anion exchange system; (ii) a DIDS-sensitive and anion-dependent K⁺ transport system, and (iii) K⁺ channels.

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Volume-responsive sodium and proton movements in dog red blood cells.

Cited by 82 publications

References 23 publications

Control of cell volume and ion transport by beta‐adrenergic 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.

Volume changes in activated human neutrophils: The role of Na⁺/H⁺ exchange

HgCI<sub>2</sub>-lnduced Ion Transport Pathways in Ehrlich Ascites Tumor Cells

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Volume-responsive sodium and proton movements in dog red blood cells.

Cited by 82 publications

References 23 publications

Control of cell volume and ion transport by beta‐adrenergic 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.

Volume changes in activated human neutrophils: The role of Na+/H+ exchange

HgCI<sub>2</sub>-lnduced Ion Transport Pathways in Ehrlich Ascites Tumor Cells

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Volume changes in activated human neutrophils: The role of Na⁺/H⁺ exchange