scholarly journals Activation of electroneutral K flux in Amphiuma red blood cells by N-ethylmaleimide. Distinction between K/H exchange and KCl cotransport.

1987 ◽  
Vol 90 (2) ◽  
pp. 209-227 ◽  
Author(s):  
J S Adorante ◽  
P M Cala
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Driving Force ◽  
Flow Analysis ◽  
Cell Swelling ◽  
Direct Effects ◽  
Kcl Cotransport ◽  
Thermodynamic Forces ◽  
Exchange Flux ◽  
Stimulation Of

Exposure of Amphiuma red blood cells to millimolar concentrations of N-ethylmaleimide (NEM) resulted in net K loss. In order to determine whether net K loss was conductive or was by electroneutral K/H exchange or KCl cotransport, studies were performed evaluating K flux in terms of the thermodynamic forces to which K flux by the above pathways should couple. The direction and magnitude of the NEM-induced net K flux did not correspond with the direction and magnitude of the forces relevant to K conductance or electroneutral KCl cotransport. Both the magnitude and direction of the NEM-activated K flux responded to the driving force for K/H exchange. We therefore conclude that NEM-induced K loss, like that by osmotically swollen Amphiuma red blood cells, is by an electroneutral K/H exchanger. In addition to the above studies, we evaluated the kinetic behavior of the volume- and NEM-induced K/H exchange flux pathways in media where Cl was replaced by SCN, NO3, para-aminohippurate (PAH), or gluconate. The anion replacement studies did not permit a distinction between K/H exchange and KCl cotransport, since, depending upon the anion used as a Cl replacement, partial inhibition or stimulation of volume-activated K/H exchange fluxes was observed. In contrast, all anions used were stimulatory to the NEM-induced K loss. Since, on the basis of force-flow analysis, both volume-and NEM-induced K loss are K/H exchange, it was necessary to reevaluate assumptions (i.e., anions serve as substrates and therefore probe the translocation step) associated with the use of anion replacement as a means of flux route identification. When viewed together with the force-flow studies, the Cl replacement studies suggest that anion effects upon K/H exchange are indirect. The different anions appear to alter mechanisms that couple NEM exposure and cell swelling to the activation of K/H exchange, as opposed to exerting direct effects upon K and H translocation.

Volume-responsive sodium movements in dog red blood cells

1983 ◽  
Vol 244 (5) ◽  
pp. C324-C330 ◽  
Author(s):  
J. C. Parker
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Cell Swelling ◽  
Cell Shrinkage ◽  
Ph Change ◽  
Sodium Permeability ◽  
Sodium Gradient ◽  
Sodium Flux ◽  
Sodium Hydrogen Exchanger

As dog red blood cells are shrunken in vitro, their sodium permeability increases progressively. Some new features of this volume-responsive transport process are described. Retardation of sodium movements in shrunken cells occurs when chloride is replaced by the more conductive anions: nitrate or thiocyanate. Micromolar concentrations of amiloride or quinidine inhibit the increment of sodium flux associated with a reduction in cell volume. In the presence of a large outwardly directed sodium gradient, dog red blood cells can progressively alkalinize the medium in which they are suspended. This pH change is stimulated by cell shrinkage, reversed by cell swelling, retarded when chloride is replaced by nitrate or thiocyanate, and inhibited by micromolar concentrations of amiloride or quinidine. The similarities between the shrinkage-associated sodium flux and the alkalinization phenomenon suggest that the mechanism responsible for increased sodium permeability in shrunken cells can be made to operate as a sodium-hydrogen exchanger.

Adenosine causes cAMP-dependent activation of chick embryo red cell carbonic anhydrase and 2,3-DPG synthesis

1996 ◽  
Vol 271 (4) ◽  
pp. R973-R981 ◽  
Author(s):  
S. Glombitza ◽  
S. Dragon ◽  
M. Berghammer ◽  
M. Pannermayr ◽  
R. Baumann
Keyword(s):  
Carbonic Anhydrase ◽  
Red Blood Cells ◽  
Adenylyl Cyclase ◽  
Adenosine Receptor ◽  
Blood Cells ◽  
Cell Protein ◽  
Red Cell ◽  
Receptor Stimulation ◽  
2,3 Dpg ◽  
Stimulation Of

In late chick embryos, coordinate activation of red cell carbonic anhydrase II (CAII) and 2,3-diphosphoglycerate (2,3-DPG) synthesis is initiated by hypoxia. The effects are mediated by unidentified hormonal effectors resident in chick plasma. In the present investigation, we have analyzed the effect of adenosine receptor stimulation on embryonic red cell CAII and 2,3-DPG synthesis. We find that primitive and definitive embryonic red blood cells from chick have an A2a adenosine receptor. Stimulation of the receptor with metabolically stable adenosine analogues causes a large increase of red cell adenosine 3',5'-cyclic monophosphate (cAMP) and subsequent activation of red cell CAII and 2,3-DPG production in definitive red blood cells and of CAII synthesis in primitive red blood cells. Direct stimulation of adenylyl cyclase with forskolin has the same effect. Analysis of red cell protein pattern after labeling with [35S]methionine shows that stimulation of red cell cAMP levels activates synthesis of several other proteins aside from CAII. Presence of actinomycin D inhibits cAMP-dependent changes of protein synthesis, indicating that cAMP-dependent transcriptional activation is required. In contrast to the stable adenosine receptor analogues, adenosine itself was a very weak agonist, unless its metabolism was significantly inhibited. Thus, besides adenosine, other effectors of the adenylyl cyclase system are likely to be involved in the O2 pressure-dependent regulation of red cell metabolism in late development of avian embryos.

Volume-dependent K+ transport in rabbit red blood cells comparison with oxygenated human SS cells

1989 ◽  
Vol 257 (1) ◽  
pp. C114-C121 ◽  
Author(s):  
N. al-Rohil ◽  
M. L. Jennings
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Cell Volume Regulation ◽  
Sulfhydryl Group ◽  
Cell Swelling ◽  
Inhibitory Potency ◽  
Ph Optimum ◽  
The Relationship ◽  
Low K ◽  
K Transport

In this study the volume-dependent or N-ethylmaleimide (NEM)-stimulated, ouabain-insensitive K+ influx and efflux were measured with the tracer 86Rb+ in rabbit red blood cells. The purpose of the work was to examine the rabbit as a potential model for cell volume regulation in human SS red blood cells and also to investigate the relationship between the NEM-reactive sulfhydryl group(s) and the signal by which cell swelling activates the transport. Ouabain-resistant K+ efflux and influx increase nearly threefold in cells swollen hypotonically by 15%. Pretreatment with 2 mM NEM stimulates efflux 5-fold and influx 10-fold (each measured in an isotonic medium). The ouabain-resistant K+ efflux was dependent on the major anion in the medium. The anion dependence of K+ efflux in swollen or NEM-stimulated cells was as follows: Br- greater than Cl- much greater than NO3- = acetate. The magnitudes of both the swelling- and the NEM-stimulated fluxes are much higher in young cells (density separated but excluding reticulocytes) than in older cells. Swelling- or NEM-stimulated K+ efflux in rabbit red blood cells was inhibited 50% by 1 mM furosemide, and the inhibitory potency of furosemide was enhanced by extracellular K+, as is known to be true for human AA and low-K+ sheep red blood cells. The swelling-stimulated flux in both rabbit and human SS cells has a pH optimum at approximately 7.4. We conclude that rabbit red blood cells are a good model for swelling-stimulated K+ transport in human SS cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Osmolyte channel regulation by ionic strength in skate RBC

2000 ◽  
Vol 279 (1) ◽  
pp. R69-R76 ◽  
Author(s):  
Kathleen A. Wittels ◽  
Elise M. Hubert ◽  
Mark W. Musch ◽  
Leon Goldstein
Keyword(s):  
Enzyme Activity ◽  
Ionic Strength ◽  
Blood Cells ◽  
Electrolyte Concentration ◽  
Cell Swelling ◽  
Channel Activity ◽  
Channel Regulation ◽  
Taurine Efflux ◽  
Stimulation Of ◽  
In Cells

The aim of this study was to determine whether the opening of the osmolyte channel in skate red blood cells (RBC) is regulated by intracellular electrolyte concentration and conductivity. Consistent with previous studies, experiments with hyperosmotic preincubation before cell swelling or swelling with an isosmotic electrolyte (e.g., ammonium chloride) showed that an increase in ionic strength inhibits the opening of the taurine channel. However, a decrease in intracellular ionic strength did not always stimulate taurine efflux to the same degree. Whereas hyposmotic swelling caused a large increase in taurine efflux, swelling induced by treatment with isosmotic nonelectrolytes produced much smaller stimulation. Results with assays for band 3 phosphorylating enzymes were consistent with those from the taurine efflux studies; stimulation of enzyme activity was lower in cells that were swollen with isosmotic nonelectrolyte media than in cells swollen in hyposmotic media. These results indicate that a decrease in ionic strength is not the only signal for the opening of the taurine channel in skate RBC. Ionic strength does affect channel activity, but there must also be some other regulator.

scholarly journals Photostimulation of lymphatic clearance of red blood cells from the mouse brain after intraventricular hemorrhage

2020 ◽  
Author(s):  
Dong-Yu Li ◽  
Shao-Jun Liu ◽  
Ting-Ting Yu ◽  
Zhang Liu ◽  
Si-Lin Sun ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Intraventricular Hemorrhage ◽  
Therapeutic Effects ◽  
Invasive Therapy ◽  
Non Invasive ◽  
Clearing Functions ◽  
Promising Therapeutic Target ◽  
Fatal Form ◽  
Stimulation Of

AbstractIntraventricular hemorrhage (IVH) is the most fatal form of brain injury, yet a therapy directed at ameliorating intraventricular clot is very limited. There is accumulating evidence that an augmentation of the meningeal lymphatic (MLVs) functions might be a promising therapeutic target for IVH. In particular, the photostimulation (PS) of MLVs could be promising for non-invasive therapy of IVH via PS of clearance of red blood cells (RBCs) from the brain via MLVs. Indeed, we uncover that PS has therapeutic effects on IVH in mice reducing the mortality, improving the emotional status, accelerating the RBCs evacuation from the ventricles and increasing the ICP recovery. Our findings strongly suggest that the PS-mediated stimulation of drainage and clearing functions of MLVs can be a novel bedside, readily applicable and commercially viable technologies for treatment of IVH. These pilot results open new horizons in a non-invasive therapy of IVH via PS stimulation of regenerative lymphatic mechanisms.

Stimulation of K-C1 cotransport in rat red cells by a hemolytic anemia-producing metabolite of dapsone

1989 ◽  
Vol 256 (2) ◽  
pp. C265-C272 ◽  
Author(s):  
M. Haas ◽  
J. H. Harrison
Keyword(s):  
Red Blood Cells ◽  
Hemolytic Anemia ◽  
Blood Cells ◽  
Pneumocystis Carinii ◽  
Fold Increase ◽  
Sh Groups ◽  
Splenic Uptake ◽  
Stimulation Of ◽  
In Cells

Dapsone, a sulfone compound used in the treatment of leprosy and, more recently, Pneumocystis carinii pneumonia, produces as a major side effect a hemolytic anemia. This anemia is characterized by oxidation of hemoglobin to methemoglobin and increased splenic uptake of red blood cells. Using a rat model, Grossman and Jollow (J. Pharmacol. Exp. Ther. 244: 118-125, 1988) found that dapsone hydroxylamine (DDS-NOH), a dapsone metabolite, is responsible for its hemolytic effect in vivo. DDS-NOH also promotes hemoglobin binding to SH groups on rat red cell membrane proteins (Budinsky et al., FASEB J. 2: A801, 1988). Since the binding of hemoglobin and other reagents (e.g., N-ethylmaleimide) to membrane SH groups has been associated with increased K transport in red blood cells, we examined the effect of DDS-NOH on K efflux from rat red blood cells in vitro. Cells shrink when exposed to DDS-NOH (100 microM) in media with plasma-like ionic composition. This shrinkage is prevented if extracellular K is raised to 110 mM or if intra- and extracellular Cl are replaced by methylsulfate (MeSO4), suggesting involvement of a K-Cl cotransport pathway. Indeed, 100 microM DDS-NOH produces a 4- to 5-fold increase in K efflux in cells containing Cl but less than a 2-fold increase in cells containing MeSO4. This stimulatory effect is specific for K; Na efflux is slightly inhibited by 100 microM DDS-NOH. The concentrations of DDS-NOH required for half-maximal stimulation of Cl-dependent K efflux (53 microM) is similar to its half-maximal hemolytic concentration in rats (approximately 100 microM). Furthermore, the stimulation of Cl-dependent K efflux by DDS-NOH is greater than 80% reversed by subsequent treatment of the cells with dithiothreitol, suggesting involvement of SH groups. Our results indicate that DDS-NOH exposure stimulates an apparent K-Cl cotransport in rat red blood cells, resulting in cell shrinkage under physiological ionic conditions. Since shrinkage of red blood cells renders them less deformable (Mohandas et al., J. Clin. Invest. 66: 563-573, 1980), this suggests a pathophysiological mechanism whereby DDS-NOH exposure in vivo could promote increased splenic uptake of red blood cells and hemolytic anemia.

Passive calcium movements in dog red blood cells: anion effects

1983 ◽  
Vol 244 (5) ◽  
pp. C318-C323 ◽  
Author(s):  
J. C. Parker
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Calcium Transport ◽  
Calcium Influx ◽  
Low Ph ◽  
Irreversible Change ◽  
Cell Shrinkage ◽  
Sodium Efflux ◽  
Sodium Dependent ◽  
Stimulation Of

Calcium influx in dog red blood cells was stimulated by replacing chloride in the medium with nitrate or thiocyanate. These anion effects were due to stimulation of a sodium-dependent calcium pathway, because calcium influx in the presence of nitrate or thiocyanate was 1) inhibited by external sodium, 2) dependent on internal sodium, 3) inhibited by cell shrinkage and low pH, and 4) inhibited by quinidine. All these characteristics had previously been shown to hold for calcium movements in the presence of chloride. Neither nitrate nor thiocyanate caused an irreversible change in calcium transport in the concentrations studied. Calcium-stimulated sodium efflux is stimulated when chloride is replaced by thiocyanate but not by nitrate. Several limiting features of the system are discussed, which preclude a conclusive interpretation of the data. The possibility is considered that the rates of sodium-dependent calcium transport in the presence of chloride, nitrate, and thiocyanate are a function of the conductance of these anions.

Sign in / Sign up

Export Citation Format

Share Document