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.

scholarly journals Coordinated control of volume regulatory Na+/H+ and K+/H+ exchange pathways in Amphiuma red blood cells

2010 ◽  
Vol 298 (3) ◽  
pp. C510-C520 ◽  
Author(s):  
Alejandro Ortiz-Acevedo ◽  
Robert R. Rigor ◽  
Hector M. Maldonado ◽  
Peter M. Cala
Keyword(s):  
Red Blood Cells ◽  
Cell Volume ◽  
Blood Cells ◽  
Coordinated Control ◽  
Cell Swelling ◽  
Cell Shrinkage ◽  
Relaxation Kinetic ◽  
Shrinkage And Swelling ◽  
Final Steady State ◽  
Single Exponential Function

The Na+/H+ and K+/H+ exchange pathways of Amphiuma tridactylum red blood cells (RBCs) are quiescent at normal resting cell volume yet are selectively activated in response to cell shrinkage and swelling, respectively. These alkali metal/H+ exchangers are activated by net kinase activity and deactivated by net phosphatase activity. We employed relaxation kinetic analyses to gain insight into the basis for coordinated control of these volume regulatory ion flux pathways. This approach enabled us to develop a model explaining how phosphorylation/dephosphorylation-dependent events control and coordinate the activity of the Na+/H+ and K+/H+ exchangers around the cell volume set point. We found that the transition between initial and final steady state for both activation and deactivation of the volume-induced Na+/H+ and K+/H+ exchange pathways in Amphiuma RBCs proceed as a single exponential function of time. The rate of Na+/H+ exchange activation increases with cell shrinkage, whereas the rate of Na+/H+ exchange deactivation increases as preshrunken cells are progressively swollen. Similarly, the rate of K+/H+ exchange activation increases with cell swelling, whereas the rate of K+/H+ exchange deactivation increases as preswollen cells are progressively shrunken. We propose a model in which the activities of the controlling kinases and phosphatases are volume sensitive and reciprocally regulated. Briefly, the activity of each kinase-phosphatase pair is reciprocally related, as a function of volume, and the volume sensitivities of kinases and phosphatases controlling K+/H+ exchange are reciprocally related to those controlling Na+/H+ exchange.

A volume-sensitive protein kinase regulates the Na-K-2Cl cotransporter in duck red blood cells

1998 ◽  
Vol 274 (4) ◽  
pp. C1002-C1010 ◽  
Author(s):  
Christian Lytle
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Inhibitory Effect ◽  
Cell Swelling ◽  
Activation Process ◽  
Calyculin A ◽  
Cell Shrinkage ◽  
Phosphorylation Event ◽  
Osmotic Cell Shrinkage ◽  
Kinetics Of

When Na-K-2Cl cotransport is activated in duck red blood cells by either osmotic cell shrinkage, norepinephrine, fluoride, or calyculin A, phosphorylation of the transporter occurs at a common set of serine/threonine sites. To examine the kinetics and regulation of the activating kinase, phosphatase activity was inhibited abruptly with calyculin A and the subsequent changes in transporter phosphorylation and activity were determined. Increases in fractional incorporation of 32P into the transporter and uptake of 86Rb by the cells were closely correlated, suggesting that the phosphorylation event is rate determining in the activation process. Observed in this manner, the activating kinase was 1) stimulated by cell shrinkage, 2) inhibited by cell swelling, staurosporine, or N-ethylmaleimide, and 3) unaffected by norepinephrine or fluoride. The inhibitory effect of swelling on kinase activity was progressively relieved by calyculin A, suggesting that the kinase itself is switched on by phosphorylation. The kinetics of activation by calyculin A conformed to an autocatalytic model in which the volume-sensitive kinase is stimulated by a product of its own reaction (e.g., via autophosphorylation).

Interactions of sodium-proton exchange mechanism in dog red blood cells with N-phenylmaleimide

1987 ◽  
Vol 253 (1) ◽  
pp. C60-C65 ◽  
Author(s):  
J. C. Parker ◽  
P. S. Glosson
Keyword(s):  
Red Blood Cells ◽  
Cell Volume ◽  
Functional Groups ◽  
Blood Cells ◽  
Proton Exchange ◽  
Cell Swelling ◽  
Cell Shrinkage ◽  
Activated State ◽  
Sodium Proton Exchange ◽  
Number Of Cells

Dog red blood cells (RBC) have a Na-H exchanger that is reversibly activated by cell shrinkage. The Na-H exchanger can be fixed in the on or off mode by treating the cells with N-phenylmaleimide. This action depends on the volume of the cells at the time of exposure to N-phenylmaleimide and also on the concentration of the reagent per number of cells. If the cells are swollen in hypotonic media during N-phenylmaleimide exposure, the Na-H exchanger becomes irreversibly inactivated, so that on subsequent shrinkage of the cells, no amiloride-sensitive Na flux is seen. This effect is maximal at N-phenylmaleimide concentrations of greater than 20 mumol/g hemoglobin. If the cells are shrunken in hypertonic media during N-phenylmaleimide exposure, the response of the Na-H exchanger depends critically on the concentration of the reagent. At N-phenylmaleimide concentrations of less than 20 mumol/g hemoglobin, the Na-H exchanger is fixed in the activated state, so that even when the volume stimulus is removed by subsequent cell swelling, an amiloride-sensitive flux is seen. Higher concentrations of N-phenylmaleimide applied to shrunken cells inhibit the Na-H exchanger. The results are accounted for in a model that envisions a volume-responsive switching mechanism for Na-H exchange that has two functional groups capable of reacting with N-phenylmaleimide. The accessibility of these groups is determined by cell volume.

Volume regulation by Amphiuma red blood cells: cytosolic free Ca and alkali metal-H exchange

1986 ◽  
Vol 250 (3) ◽  
pp. C423-C429 ◽  
Author(s):  
P. M. Cala ◽  
L. J. Mandel ◽  
E. Murphy
Keyword(s):  
Alkali Metal ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Volume Regulation ◽  
Null Point ◽  
Cell Swelling ◽  
Maximal Concentration ◽  
Cell Shrinkage ◽  
Osmotic Swelling ◽  
Intracellular Ca

Osmotic swelling of Amphiuma red blood cells results in activation of electroneutral K-H exchange, whereas cell shrinkage activates an electroneutral Na-H exchange. These K-H and Na-H exchangers function to restore cell volume to normal after cell swelling and shrinkage, respectively. Our previous studies have suggested that Ca plays a role in volume-dependent activation of K-H exchange. In the present studies, intracellular free Ca levels were measured employing the Ca-sensitive extracellular dye arsenazo III and a previously described null-point method. Control values for intracellular free Ca averaged 0.46 +/- 0.15 microM. Cell shrinkage caused this value to decrease to 0.16 +/- 0.11 microM, whereas either cell swelling or addition of 5 microM A23187 resulted in saturation of intracellular Ca buffers, suggesting that both treatments caused an increase in intracellular free Ca. In the presence of 7 microM A23187, the rate of K-H exchange displayed a hyperbolic relationship as a function of extracellular Ca (Cao). The apparent half-maximal concentration for Cao (in the presence of 7 microM A23187) was 0.27 mM for osmotically swollen cells and 1.9 mM for cells in isotonic medium, suggesting that the Ca affinity of a modulating site is increased in swollen cells. Inhibitors of Ca-mediated processes, such as quinidine and the phenothiazines, inhibited K-H exchange. In contrast, the phenothiazines chlorpromazine and trifluoperazine stimulated Na-H exchange by osmotically shrunken cells. These results suggest that increases in intracellular free Ca are involved in stimulating K-H exchange while repressing Na-H exchange in Amphiuma red blood cells.

Ultrastructural observations on the in vitro cytoadherence of Plasmodium falciparum infected red blood cells

1990 ◽  
Vol 48 (3) ◽  
pp. 914-915
Author(s):  
D.J.P. Ferguson ◽  
A.R. Berendt ◽  
J. Tansey ◽  
K. Marsh ◽  
C.I. Newbold
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Umbilical Vein ◽  
Cell Types ◽  
Amelanotic Melanoma ◽  
Cytoplasmic Process ◽  
Umbilical Vein Endothelial Cells

In human malaria, the most serious clinical manifestation is cerebral malaria (CM) due to infection with Plasmodium falciparum. The pathology of CM is thought to relate to the fact that red blood cells containing mature forms of the parasite (PRBC) cytoadhere or sequester to post capillary venules of various tissues including the brain. This in vivo phenomenon has been studied in vitro by examining the cytoadherence of PRBCs to various cell types and purified proteins. To date, three Ijiost receptor molecules have been identified; CD36, ICAM-1 and thrombospondin. The specific changes in the PRBC membrane which mediate cytoadherence are less well understood, but they include the sub-membranous deposition of electron-dense material resulting in surface deformations called knobs. Knobs were thought to be essential for cytoadherence, lput recent work has shown that certain knob-negative (K-) lines can cytoadhere. In the present study, we have used electron microscopy to re-examine the interactions between K+ PRBCs and both C32 amelanotic melanoma cells and human umbilical vein endothelial cells (HUVEC).We confirm previous data demonstrating that C32 cells possess numerous microvilli which adhere to the PRBC, mainly via the knobs (Fig. 1). In contrast, the HUVEC were relatively smooth and the PRBCs appeared partially flattened onto the cell surface (Fig. 2). Furthermore, many of the PRBCs exhibited an invagination of the limiting membrane in the attachment zone, often containing a cytoplasmic process from the endothelial cell (Fig. 2).

Effect of liposomal curcumin on red blood cells in vitro

2013 ◽  
Vol 1 (Suppl. 1) ◽  
pp. A4.1
Author(s):  
Angela Storka
Keyword(s):  
Red Blood Cells ◽  
Blood Cells

scholarly journals THE SYNTHESIS OF PROTOPORPHYRIN IN VITRO BY RED BLOOD CELLS OF THE DUCK

1950 ◽  
Vol 183 (2) ◽  
pp. 757-765 ◽  
Author(s):  
David Shemin ◽  
Irving M. London ◽  
D. Rittenberg
Keyword(s):  
Red Blood Cells ◽  
Blood Cells

Nucleated red blood cells participate in myocardial regeneration in the toad Bufo Gargarizan Gargarizan

2021 ◽  
pp. 153537022110132
Author(s):  
Shu-Qin Liu ◽  
Xiao-Ye Hou ◽  
Feng Zhao ◽  
Xiao-Ge Zhao
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Cardiac Injury ◽  
Myocardial Regeneration ◽  
Matrix Metalloproteinase 2 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cardiac Tissues ◽  
Nucleated Red Blood Cells ◽  
Model Animal

Heart regeneration is negligible in humans and mammals but remarkable in some ectotherms. Humans and mammals lack nucleated red blood cells (NRBCs), while ectotherms have sufficient NRBCs. This study used Bufo gargarizan gargarizan, a Chinese toad subspecies, as a model animal to verify our hypothesis that NRBCs participate in myocardial regeneration. NRBC infiltration into myocardium was seen in the healthy toad hearts. Heart needle-injury was used as an enlarged model of physiological cardiomyocyte loss. It recovered quickly and scarlessly. NRBC infiltration increased during the recovery. Transwell assay was done to in vitro explore effects of myocardial injury on NRBCs. In the transwell system, NRBCs could infiltrate into cardiac pieces and could transdifferentiate toward cardiomyocytes. Heart apex cautery caused approximately 5% of the ventricle to be injured to varying degrees. In the mildly to moderately injured regions, NRBC infiltration increased and myocardial regeneration started soon after the inflammatory response; the severely damaged region underwent inflammation, scarring, and vascularity before NRBC infiltration and myocardial regeneration, and recovered scarlessly in four months. NRBCs were seen in the newly formed myocardium. Enzyme-linked immunosorbent assay and Western blotting showed that the levels of tumor necrosis factor-α, interleukin- 1β, 6, and11, cardiotrophin-1, vascular endothelial growth factor, erythropoietin, matrix metalloproteinase- 2 and 9 in the serum and/or cardiac tissues fluctuated in different patterns during the cardiac injury-regeneration. Cardiotrophin-1 could induce toad NRBC transdifferentiation toward cardiomyocytes in vitro. Taken together, the results suggest that the NRBC is a cell source for cardiomyocyte renewal/regeneration in the toad; cardiomyocyte loss triggers a series of biological processes, facilitating NRBC infiltration and transition to cardiomyocytes. This finding may guide a new direction for improving human myocardial regeneration.

scholarly journals Multimodal Diagnostics of Microrheologic Alterations in Blood of Coronary Heart Disease and Diabetic Patients

Diagnostics ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 76
Author(s):  
Anastasia Maslianitsyna ◽  
Petr Ermolinskiy ◽  
Andrei Lugovtsov ◽  
Alexandra Pigurenko ◽  
Maria Sasonko ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Optical Methods ◽  
Diabetic Patients ◽  
Aggregation Index ◽  
Significant Difference

Coronary heart disease (CHD) has serious implications for human health and needs to be diagnosed as early as possible. In this article in vivo and in vitro optical methods are used to study blood properties related to the aggregation of red blood cells in patients with CHD and comorbidities such as type 2 diabetes mellitus (T2DM). The results show not only a significant difference of the aggregation in patients compared to healthy people, but also a correspondence between in vivo and in vitro parameters. Red blood cells aggregate in CHD patients faster and more numerously; in particular the aggregation index increases by 20 ± 7%. The presence of T2DM also significantly elevates aggregation in CHD patients. This work demonstrates multimodal diagnostics and monitoring of patients with socially significant pathologies.

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