Low potassium-type but not high potassium-type sheep red blood cells show passive K+ transport induced by low ionic strength

1991 ◽  
Vol 1061 (1) ◽  
pp. 85-88 ◽  
Author(s):  
Andreas Erdmann ◽  
Ingolf Bernhardt ◽  
Steven J. Pittman ◽  
J. Clive Ellory
1971 ◽  
Vol 57 (5) ◽  
pp. 593-609 ◽  
Author(s):  
Robert B. Gunn ◽  
Daniel C. Tosteson

2,4,6-Trinitro-3-methyl-phenol (trinitrocresol, H+TNC-) was found to inhibit anion and stimulate cation movements across the membranes of both high potassium (HK) and low potassium (LK) sheep red blood cells. The concentration of TNC- required to inhibit SO4- and Cl- efflux (10-5-10-3 M) was less than that required to increase Na+ and K+ leakage (10-3-10-2 M). Both the inhibition of anion and stimulation of cation permeation were reversed if TNC- was washed from the red cells. The cation leak caused by TNC- was much greater at 0° and 37°C than at room temperature (23°C). In sheep red cells, TNC- was found to be about 20 times more effective than salicylate and about 40 times more effective than thiocyanate in increasing cation leak. TNC- also inhibited the ouabain-sensitive potassium influx.


2021 ◽  
Vol 2 (3) ◽  
pp. 139-168
Author(s):  
GF Fuhrmann ◽  
KJ Netter

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.


1990 ◽  
Vol 258 (6) ◽  
pp. C1169-C1172 ◽  
Author(s):  
J. A. Halperin ◽  
C. Brugnara ◽  
T. Van Ha ◽  
D. C. Tosteson

We have recently reported that voltage-activated fluxes of Na, K, and Ca occur in human red blood cells [J.A. Halperin, C. Brugnara, M. Tosteson, T. Van Ha, and D. C. Tosteson. Am. J. Physiol. 257 (Cell Physiol. 26): C986-C996, 1989]. The cation permeability increases progressively as the membrane potential becomes more inside positive above +20 mV. In this paper we show that this effect also occurs in high-potassium (HK), but not in low-potassium (LK), sheep and dog red blood cells. This result suggests that the voltage-activated cation transport pathway is not the result of nonspecific dielectric breakdown of the lipid bilayer but, rather, relates to some membrane component, presumably a protein, that is expressed in HK human and sheep but not in LK sheep and dog red blood cells.


1974 ◽  
Vol 64 (5) ◽  
pp. 536-550 ◽  
Author(s):  
John R. Sachs ◽  
Philip B. Dunham ◽  
Donna L. Kropp ◽  
J. Clive Ellory ◽  
Joseph F. Hoffman

The characteristics of the interaction of Na-K pumps of high potassium (HK) and low potassium (LK) goat red blood cells with ouabain have been determined. The rate of inhibition by ouabain of the pump of HK cells is greater than the rate of inhibition of the pumps of LK cells. Treatment of LK cells with an antibody (anti-L) raised in HK sheep by injecting LK sheep red cells increases the rate of inhibition of the LK pumps by ouabain to that characteristic of HK pumps; reduction of intracellular K (Kc) in LK cells increases the rate at which ouabain inhibits their pumps and exposure of these low Kc cells to anti-L does not affect the rate of inhibition. There is considerable heterogeneity in the pumps of both HK and LK cells in the rate at which they interact with ouabain or the rate at which they pump or both. LK pumps which are sensitive to stimulation by anti-L bind ouabain less rapidly than the remainder of the LK pumps and exposure to antibody increases the rate at which ouabain binds to the sensitive pumps; the difference between the two types of pumps disappears if intracellular K is very low. The calculated number of ouabain molecules bound at 100% inhibition of the pump is about the same for HK and LK cells. Although exposure to anti-L increases the apparent number of ouabain binding sites in LK cells at normal Kc, it does not alter the apparent number of sites in LK cells when Kc has been reduced.


1986 ◽  
Vol 250 (1) ◽  
pp. C55-C64 ◽  
Author(s):  
J. S. Adorante ◽  
R. I. Macey

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.


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