scholarly journals Transmembrane Potential of Red Blood Cells Under Low Ionic Strength Conditions

2013 ◽  
Vol 31 (6) ◽  
pp. 875-882 ◽  
Author(s):  
Daniel Moersdorf ◽  
Stephane Egee ◽  
Claudia Hahn ◽  
Benjamin Hanf ◽  
Clive Ellory ◽  
...  
Keyword(s):  
Ionic Strength ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Transmembrane Potential ◽  
Low Ionic Strength

scholarly journals A Hundred-Year Researching History on the Low Ionic Strength in Red Blood Cells: Literature Review

2021 ◽  
Vol 2 (3) ◽  
pp. 139-168
Author(s):  
GF Fuhrmann ◽  
KJ Netter
Keyword(s):  
Membrane Potential ◽  
Ionic Strength ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Sucrose Solution ◽  
Critical Survey ◽  
Unequal Distribution ◽  
Donnan Equilibrium ◽  
Disulfonic Stilbene ◽  
Low Ionic Strength

This review article provides a critical survey of work from 1904 to 2003 on the effects of low ionic strength in Red Blood Cells (RBCs) incubated in media with impermeable sugars such as sucrose. In 1904 Gürber A washed RBCs of different species with isotonic sucrose solution to eliminate the outside ions in order to better analyse their intracellular ionic composition; however, this approach was not feasible because of a substantial salt efflux from the cells. A prominent feature of the salt loss is the shrinking of the RBCs. A central role in the understanding of the ionic movements is thereby the new Donnan equilibrium of the anions. Experimental evidence has been given by Jacobs MH and Parpart AK in 1933. In the sucrose medium two phases could be predicted: 1) a very rapid anionic shift resulting in an unequal distribution of chloride and hydroxyl anions on both sides of the membrane and 2) a leakage of salts from the RBCs. In 1940 Wilbrandt W assumed that a positive membrane potential is in line with the salt loss at low ionic strength in RBCs. In 1977 Knauf PA, Fuhrmann GF, Rothstein S and Rothstein A observed in RBCs an inhibition of both, anion exchange and also of net anion efflux, by incubation with disulfonic stilbene derivates. At low ionic strength the Donnan equilibrium is immediately obtained by the Anion Exchanger Protein (AEP). The resulting positive membrane potential opens at least two new types of cation pores or channels. Thereby is the conductivity pathway for the anions, namely the AEP, in charge of the net anion loss at low ionic strength. The AEP pathway is extensively blocked by disulfonic stilbene compounds. The permeability ways for cations through these pores or channels are not yet explored.

Calcium-induced transient potassium efflux in human red blood cells

1986 ◽  
Vol 250 (1) ◽  
pp. C55-C64 ◽  
Author(s):  
J. S. Adorante ◽  
R. I. Macey
Keyword(s):  
Ionic Strength ◽  
Phase I ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Potassium Efflux ◽  
Pump Failure ◽  
Human Red Blood Cells ◽  
Low Ionic Strength ◽  
Low K ◽  
Phase Phase

Human red blood cells pretreated with low-ionic-strength solutions and resuspended in saline respond biphasically to extracellular Ca. At first, addition of Ca causes a large transient K efflux of as much as 600 mM . liter cell H2O-1 . h-1; this is followed by a decrease in K flux below control levels. The first phase (phase I) resembles the Gardos effect in several respects. It is inhibited by oligomycin, by external K, and by increased exposure time to Ca. Further, the K permeability of phase I is similar to that of the Gardos effect (5 X 10(-8)-9 X 10(-8) cm/s), and the cells hyperpolarize in a low-K medium when Ca2+ is added. However, phase I is not identical to the Gardos phenomenon. For example, La, which prevents the Gardos response, is ineffective on phase I. Moreover, external Ba prevents the development of phase I but not the Gardos response, whereas internal Ba prevents the Gardos response. Attempts to demonstrate a Ca leak or pump failure during phase I have failed; passive Ca movements of both treated and normal cells are similar. The results suggest that low-ionic-strength solution exposes Ca-sensitive sites to the external medium; these sites are maintained when the cells are returned to saline.

The influence of chlorpromazine on the potential-induced shape change of human erythrocyte

1991 ◽  
Vol 11 (4) ◽  
pp. 213-221 ◽  
Author(s):  
J. Hartmann ◽  
R. Glaser
Keyword(s):  
Red Blood Cells ◽  
Human Erythrocyte ◽  
Blood Cells ◽  
Characteristic Time ◽  
Time Course ◽  
Transmembrane Potential ◽  
Shape Change ◽  
Human Erythrocytes

The effect of chlorpromazine (CPZ) on the shape of human erythrocytes with different values of transmembrane potential (TMP) was investigated. The shape of red blood cells with negative values of the TMP remained unchanged after the formation of stomatocytes by chlorpromazine, while cells with positive TMP showed a characteristic time course of shape change during the incubation with CPZ. Experiments with vanadate show that this might be due to a difference in the activity of the phospholipid-translocase at different values of TMP.

Defining the volume dependence of multiple K flux pathways of trout red blood cells

1997 ◽  
Vol 272 (4) ◽  
pp. C1099-C1111 ◽  
Author(s):  
M. Berenbrink ◽  
Y. R. Weaver ◽  
A. R. Cossins
Keyword(s):  
Ionic Strength ◽  
Red Blood Cells ◽  
Ammonium Chloride ◽  
Blood Cells ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Graded Responses ◽  
Volume Dependence ◽  
Volume Sensitivity ◽  
The Relationship

The volume sensitivity of different K flux pathways has been determined in trout red blood cells subjected to volume perturbation. Gentle hyposmotic swelling induced a K influx in a Cl-containing saline but not in NO3- or methanesulfonate (MeSF)-containing salines, consistent with the activation of a Cl-dependent flux. Extreme hyposmotic swelling led to larger K fluxes in all salines but with reduced anion discrimination of the Cl-dependent flux. In contrast to these graded responses, isosmotic swelling using ammonium chloride or beta-adrenergic stimulation activated only Cl-dependent fluxes in an all-or-none fashion. The relationship between the hyposmotically and isosmotically induced pathways was studied by coactivation using either ammonium chloride or isoproterenol with anisosmotic treatment. Cells in ammonium chloride-containing hyposmotic salines showed no additive K flux over that induced by hyposmotic treatment alone, indicating that the isosmotically induced Cl-dependent flux was identical to the hyposmotically induced Cl-dependent flux. However, cells coactivated by hyposmotic and beta-adrenergic treatment showed a small Cl-dependent flux in addition to that induced by hyposmotic treatment alone. This small third component was unaffected by anisosmotic treatment. We conclude that the major Cl-dependent and Cl-independent K flux pathways are distinct and separate and that the former has an anion dependence that varies with cell volume and a volume sensitivity that varies with ionic strength.

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