Transport of water and urea in red blood cells

1984 ◽  
Vol 246 (3) ◽  
pp. C195-C203 ◽  
Author(s):  
R. I. Macey
Keyword(s):  
Red Blood Cells ◽  
Lipid Bilayers ◽  
Blood Cells ◽  
Renal Medulla ◽  
Water Channels ◽  
Facilitated Diffusion ◽  
Red Cell Membrane ◽  
Single File ◽  
Osmotic Stability ◽  
Water Transport Properties

Evidence for water channels in red blood cells is reviewed. In an entropically driven reaction, organic mercurials decrease water permeability, elevate the activation energy, and reduce the ratio of osmotic to diffusional water permeabilities to unity so that water transport properties of red blood cells are hardly distinguishable from lipid bilayers. It is concluded that mercurials close the water channels. A variety of kinetic, pharmacological, and comparative evidence converges on the conclusion that urea and other solutes are excluded from water channels. Urea apparently permeates the red cell membrane via a facilitated diffusion system, which plays an important role when red blood cells traverse the renal medulla; rapid urea transport helps preserve the osmotic stability and deformability of the cell, and it helps prevent dissipation of extracellular osmotic gradients. Water apparently traverses the channel via a single-file mechanism; the very low channel permeability of H+ is explained if the channel contains fixed charge, or alternatively, if the mobile water molecules within the channel do not form a continuum. An alternative unitary pore hypothesis for simultaneous transport of water, ions, and small solutes is also discussedl.

scholarly journals Hemoglobin Oxidation in Stored Blood Accelerates Hemolysis and Oxidative Injury to Red Blood Cells

2020 ◽  
Vol 12 (04) ◽  
pp. 244-249
Author(s):  
Ibrahim Mustafa ◽  
Tameem Ali Qaid Hadwan
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Morphological Changes ◽  
Hemoglobin Concentration ◽  
Red Cell Membrane ◽  
Rbc Membrane ◽  
Hemoglobin Oxidation ◽  
Rbc Indices ◽  
Methemoglobin Formation ◽  
Stored Blood

Abstract Introduction Maintaining blood supply is a challenge in blood banks. Red blood cells (RBCs) stored at 4°C experience issues of biochemical changes due to metabolism of cells, leading to changes collectively referred to as “storage lesions.” Oxidation of the red cell membrane, leading to lysis, contributes to these storage lesions. Methods Blood bags with CPD-SAGM stored at 4°C for 28 days were withdrawn aseptically on days 1, 14, and 28. Hematology analyzer was used to investigate RBC indices. Hemoglobin oxidation was studied through spectrophotometric scan of spectral change. RBC lysis was studied with the help of Drabkin's assay, and morphological changes were observed by light and scan electron microscopy. Results RBCs show progressive changes in morphology echinocytes and spherocytes on day 28. There was 0.85% RBC lysis, an approximately 20% decrease in percentage oxyhemoglobin, and a 14% increase in methemoglobin formation, which shows hemoglobin oxidation on day 28. Conclusions Oxidative damage to RBC, with an increase in storage time was observed in the present study. The observed morphological changes to RBC during the course of increased time shows that there is progressive damage to RBC membrane and a decrease in hemoglobin concentration; percentage RBC lysis is probably due to free hemoglobin and iron.

Osmotic stability of red cells in renal circulation requires rapid urea transport

1988 ◽  
Vol 254 (5) ◽  
pp. C669-C674 ◽  
Author(s):  
R. I. Macey ◽  
L. W. Yousef
Keyword(s):  
Lipid Bilayers ◽  
Physiological Role ◽  
Renal Medulla ◽  
Red Cells ◽  
Facilitated Diffusion ◽  
Urea Transport ◽  
Permeability Characteristics ◽  
Cortex Cell ◽  
Cell Stability ◽  
Michaelis Constants

Urea transport by the human erythrocyte occurs via an asymmetric-facilitated diffusion system with high Michaelis constants and high maximal velocities; the equivalent permeability in the limit of zero urea concentration is approximately 10(-3) cm/s (J. Gen. Physiol. 81: 221-237, 239-253, 1983). A physiological role for this system is revealed by numerical integration of the appropriate equations that show that rapid urea transport is essential for red cell stability in passing through the renal medulla. The calculation compares two cells. Cell A transports urea with permeability characteristics of normal red cells; cell B has urea permeability similar to lipid bilayers. On entering the hypertonic medulla, both cells shrink, but only B swells on leaving the medulla. The osmotic stress for cell B is greater than for A. Cell B is close to hypertonic hemolysis in the medulla and to hypotonic hemolysis in the cortex. Cell B remains swollen for some time after its exit; the resulting decreased deformability presents a hazard if B reenters the microcirculation. Furthermore, cell B removes a significant fraction of the filtered load of urea and compromises the osmotic gradients in the medulla.

scholarly journals Molecular interactions of mefenamic acid with lipid bilayers and red blood cells

2011 ◽  
Vol 22 (12) ◽  
pp. 2243-2249 ◽  
Author(s):  
Mario Suwalsky ◽  
Marcela Manrique-Moreno ◽  
Jörg Howe ◽  
Klaus Brandenburg ◽  
Fernando Villena
Keyword(s):  
Red Blood Cells ◽  
Lipid Bilayers ◽  
Molecular Interactions ◽  
Mefenamic Acid ◽  
Blood Cells

The squeezing of red blood cells through capillaries with near-minimal diameters

1989 ◽  
Vol 203 ◽  
pp. 381-400 ◽  
Author(s):  
D. Halpern ◽  
T. W. Secomb
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Cell Shape ◽  
Numerical Solutions ◽  
Tube Diameter ◽  
Red Cells ◽  
Rheological Parameters ◽  
Red Cell ◽  
Red Cell Membrane ◽  
Intact Cells

An analysis is presented of the mechanics of red blood cells flowing in very narrow tubes. Mammalian red cells are highly flexible, but their deformations satisfy two significant constraints. They must deform at constant volume, because the contents of the cell are incompressible, and also at nearly constant surface area, because the red cell membrane strongly resists dilation. Consequently, there exists a minimal tube diameter below which passage of intact cells is not possible. A cell in a tube with this diameter has its critical shape: a cylinder with hemispherical ends. Here, flow of red cells in tubes with near-minimal diameters is analysed using lubrication theory. When the tube diameter is slightly larger than the minimal value, the cell shape is close to its shape in the critical case. However, the rear end of the cell becomes flattened and then concave with a relatively small further increase in the diameter. The changes in cell shape and the resulting rheological parameters are analysed using matched asymptotic expansions for the high-velocity limit and using numerical solutions. Predictions of rheological parameters are also obtained using the assumption that the cell is effectively rigid with its critical shape, yielding very similar results. A rapid decrease in the apparent viscosity of red cell suspensions with increasing tube diameter is predicted over the range of diameters considered. The red cell velocity is found to exceed the mean bulk velocity by an amount that increases with increasing tube diameter.

scholarly journals Oxidation of intracellular glutathione after exposure of human red blood cells to hypochlorous acid

1995 ◽  
Vol 307 (1) ◽  
pp. 57-62 ◽  
Author(s):  
M C M Vissers ◽  
C C Winterbourn
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Hypochlorous Acid ◽  
Low Doses ◽  
Red Cell Membrane ◽  
Human Red Blood Cells ◽  
Cell Components ◽  
Slow Infusion ◽  
Higher Doses ◽  
Selective Process

Exposure of human red blood cells to low doses of hypochlorous acid (HOCl) resulted in the loss of intracellular GSH. Oxidation occurred less than 2 min after the addition of HOCl, and required approx. 2.5 mol of HOCl per mol of GSH lost. Loss of GSH preceded oxidation of membrane thiols, the formation of chloramines and haemoglobin oxidation. The susceptibility of intracellular GSH to oxidation by HOCl was two-thirds that of GSH in cell lysates. These results indicate that HOCl can penetrate the red cell membrane, which provides little barrier protection for cytoplasmic components, and that GSH oxidation by HOCl may be a highly selective process. Virtually all of the GSH lost was converted into GSSG. If glucose was added to the medium, most of the GSH oxidized by low doses of HOCl was rapidly regenerated. At higher doses, recovery was less efficient. However, when HOCl was added as a slow infusion rather than in a single bolus, there was increased recovery at higher doses. This indicates that in metabolically active cells regeneration is rapid and GSH may protect cell components from damage by HOCl. HOCl-induced lysis was only slightly delayed by adding glucose to the medium, indicating that lytic injury is not ameliorated by GSH.

scholarly journals Cholesterol Deficiency Causes Impaired Osmotic Stability of Cultured Red Blood Cells

2019 ◽  
Vol 10 ◽  
Author(s):  
Claudia Bernecker ◽  
Harald Köfeler ◽  
Georg Pabst ◽  
Martin Trötzmüller ◽  
Dagmar Kolb ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Osmotic Stability

Hemolytic action of potassium salts on dog red blood cells

1983 ◽  
Vol 244 (5) ◽  
pp. C313-C317 ◽  
Author(s):  
J. C. Parker
Keyword(s):  
Cell Membrane ◽  
Potassium Channel ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Red Cell ◽  
Potassium Salts ◽  
Red Cell Membrane ◽  
Potassium Flux ◽  
Hemolytic Action ◽  
Calcium Activated Potassium Channel

Recent demonstrations of chloride-associated passive potassium movements in red blood cells of humans, ducks, sheep, and toadfish prompted a reinvestigation of potassium permeability in dog red blood cells. Early observations of Davson (J. Physiol. London 101:265-283, 1942) had shown that replacement of chloride by nitrate and thiocyanate caused a greatly increased rate of potassium flux across the dog red cell membrane. This finding seemed at variance with results in other species in which chloride replacement caused a fall in potassium flux. The present data indicate that passive potassium movements in swollen dog red blood cells are chloride dependent and furosemide sensitive, as shown for the cells of other species. Davson's findings were demonstrated to be due to the inclusion of small quantities of calcium in the medium under circumstances that favored calcium entry into the cells, thus opening the calcium-activated potassium channel described by Gardos (Curr. Top. Membr. Transp. 10:217-277, 1978 and Nature London 279:248-250, 1979). Potassium movements through the latter channel were stimulated when chloride was replaced by more permeant anions, such as nitrate and thiocyanate, which also increased the rate of net potassium movements in valinomycin-treated cells.

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