Iodoacetic acid inhibition of calcium-dependent potassium efflux in red blood cells

1985 ◽  
Vol 248 (5) ◽  
pp. C419-C424 ◽  
Author(s):  
G. A. Plishker
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Protein Band ◽  
Iodoacetic Acid ◽  
Specific Protein ◽  
Metabolic Inhibitor ◽  
Potassium Efflux ◽  
Calcium Dependent ◽  
Irreversible Inhibition ◽  
Cellular Ca

The metabolic inhibitor, iodoacetic acid (IAA), has commonly been used to increase Ca-dependent K efflux in red blood cells. It is thought that this effect of IAA involves the irreversible inhibition of glyceraldehyde-phosphate dehydrogenase (EC 1.2.1.12), resulting in the energy depletion of the cell. Without energy, active transport stops, and the K loss is enhanced both by increasing cellular Ca and by preventing K reuptake. The present study shows that in addition to this metabolic effect, which increases Ca-dependent K efflux, IAA also inhibits this efflux. This inhibition is irreversible and is not related to the ATP or Ca concentrations of the cells. The carboxymethylation of a specific protein band correlates with IAA inhibition of K efflux.

Involvement of a cytoplasmic protein in calcium-dependent potassium efflux in red blood cells

1986 ◽  
Vol 251 (4) ◽  
pp. C535-C540 ◽  
Author(s):  
G. A. Plishker ◽  
P. H. White ◽  
E. D. Cadman
Keyword(s):  
Calcium Concentration ◽  
Protein Band ◽  
Iodoacetic Acid ◽  
Inhibitory Effect ◽  
Cytoplasmic Protein ◽  
Potassium Efflux ◽  
Potassium Permeability ◽  
Calcium Dependent ◽  
Free Intracellular Calcium ◽  
Lines Of Evidence

The potassium permeability of the human red blood cell increases with the free intracellular calcium concentration. The efflux of potassium can be inhibited by iodoacetic acid. This inhibitory effect correlates directly with the carboxymethylation of a protein band found in both the hemolysate and membrane fractions. The present study provides two additional lines of evidence that this protein is involved directly with the calcium-dependent changes in potassium permeability: its association with the membrane is calcium dependent; and calcium-dependent potassium efflux from resealed ghost is inhibited by the incorporation of antibodies raised against this cytoplasmic protein.

Densitometric Identification of Primitive Erythroblasts After Reaction With Diaminobenzidine

1973 ◽  
Vol 31 ◽  
pp. 328-329
Author(s):  
John A. Trotter
Keyword(s):  
Red Blood Cells ◽  
Analytical Method ◽  
Blood Cells ◽  
Guinea Pigs ◽  
Specific Protein ◽  
Visual Examination ◽  
Hemoglobin Synthesis ◽  
Peroxidatic Activity ◽  
Small Density

Hemoglobin is the specific protein of red blood cells. Those cells in which hemoglobin synthesis is initiated are the earliest cells that can presently be considered to be committed to erythropoiesis. In order to identify such early cells electron microscopically, we have made use of the peroxidatic activity of hemoglobin by reacting the marrow of erythropoietically stimulated guinea pigs with diaminobenzidine (DAB). The reaction product appeared as a diffuse and amorphous electron opacity throughout the cytoplasm of reactive cells. The detection of small density increases of such a diffuse nature required an analytical method more sensitive and reliable than the visual examination of micrographs. A procedure was therefore devised for the evaluation of micrographs (negatives) with a densitometer (Weston Photographic Analyzer).

Oxidation-induced calcium-dependent dehydration of normal human red blood cells

2007 ◽  
Vol 41 (5) ◽  
pp. 536-545 ◽  
Author(s):  
Irina M. Shcherbachenko ◽  
Irina L. Lisovskaya ◽  
Vladimir P. Tikhonov
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Calcium Dependent ◽  
Human Red Blood Cells ◽  
Normal Human

Role of Non-specific Protein in the Sensitization of Red Blood Cells by Antigen

Nature ◽  
1965 ◽  
Vol 205 (4971) ◽  
pp. 610-611 ◽  
Author(s):  
MAXWELL RICHTER ◽  
JOHN COHEN
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Specific Protein

scholarly journals Role of calcium in volume regulation by dog red blood cells.

1975 ◽  
Vol 65 (1) ◽  
pp. 84-96 ◽  
Author(s):  
J C Parker ◽  
H J Gitelman ◽  
P S Glosson ◽  
D L Leonard
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Sodium Concentration ◽  
Calcium Flux ◽  
Osmotic Swelling ◽  
Calcium Dependent ◽  
Sodium Extrusion ◽  
Calcium Permeability ◽  
External Calcium

Dog red blood cells (RBC) are shown to regulate their volume in anisosmotic media. Extrusion of water from osmotically swollen cells requires external calcium and is associated with net outward sodium movement. Accumulation of water by osmotically shrunken cells is not calcium dependent and is associated with net sodium uptake. Net movements of calcium are influenced by several variables including cell volume, pH, medium sodium concentration, and cellular sodium concentration. Osmotic swelling of cells increases calcium permeability, and this effect is diminished at acid pH. Net calcium flux in either direction between cells and medium is facilitated when the sodium concentrations is low in the compartment from which calcium moves and/or high in the compartment to which calcium moves. The hypothesis is advanced that energy for active sodium extrusion in dog RBC comes from passive, inward flow of calcium through a countertransport mechanism.

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.

Prostaglandin E2 activates channel-mediated calcium entry in human erythrocytes: an indication for a blood clot formation supporting process

2004 ◽  
Vol 92 (12) ◽  
pp. 1269-1272 ◽  
Author(s):  
Wiebke Tabellion ◽  
Peter Lipp ◽  
Ingolf Bernhardt ◽  
Lars Kaestner
Keyword(s):  
Prostaglandin E2 ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Calcium Influx ◽  
Blood Clot ◽  
Clot Formation ◽  
Patch Clamp Technique ◽  
Red Cell Membrane ◽  
Potassium Efflux ◽  
Gardos Channel

SummaryProstaglandin E2 (PGE2) is released from platelets when they are activated. Using fluorescence imaging and the patch-clamp technique, we provide evidence that PGE2 at physiological concentrations (10−10 M) activates calcium rises mediated by calcium influx through a non-selective cation-channel in human red blood cells. The extent of calcium increase varied between cells with a total of 45% of the cells responding. It is well known that calcium increases elicited the calcium-activated potassium channel (Gardos channel) in the red cell membrane. Previously, it was shown that the Gardos channel activation results in potassium efflux and shrinkage of the cells. Therefore, we conclude that the PGE2 responses of red blood cells described here reveal a direct and active participation of erythrocytes in blood clot formation.

Sign in / Sign up

Export Citation Format

Share Document