scholarly journals Comparative Monovalent Cation Transport in Neonatal and Adult Red Blood Cells

1984 ◽  
Vol 18 (8) ◽  
pp. 778-780 ◽  
Author(s):  
Aixa Muller-Soyano ◽  
Bonnie W Ramsey ◽  
Bertil E Glader
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Monovalent Cation ◽  
Cation Transport

Voltage-activated cation permeability in high-potassium but not low-potassium red blood cells

1990 ◽  
Vol 258 (6) ◽  
pp. C1169-C1172 ◽  
Author(s):  
J. A. Halperin ◽  
C. Brugnara ◽  
T. Van Ha ◽  
D. C. Tosteson
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Dielectric Breakdown ◽  
Cation Transport ◽  
Membrane Component ◽  
Transport Pathway ◽  
High Potassium ◽  
Human Red Blood Cells ◽  
Cation Permeability ◽  
Low Potassium

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.

Insulin sensitivity of human red blood cells cation transport

1985 ◽  
Vol 10 ◽  
pp. 26-29 ◽  
Author(s):  
P. Baldini ◽  
M. D'Onofrio ◽  
S. Incerpi ◽  
P. Luly ◽  
C. Rinaldi ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Cation Transport ◽  
Human Red Blood Cells

scholarly journals Cation transport of red blood cells from hypertensive patients in Japan.

1983 ◽  
Vol 24 (6) ◽  
pp. 909-915
Author(s):  
Shunichi KOJIMA ◽  
Keiichi ITOH ◽  
Fujio DEGUCHI ◽  
Tsuguo OSADA ◽  
Hidenao ASHIDA ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Cation Transport ◽  
Hypertensive Patients

scholarly journals Dog Red Blood Cells

1973 ◽  
Vol 61 (2) ◽  
pp. 146-157 ◽  
Author(s):  
John C. Parker
Keyword(s):  
Red Blood Cells ◽  
Normal State ◽  
Blood Cells ◽  
Cation Transport ◽  
Red Cells ◽  
Na Pump ◽  
Donnan Equilibrium

Red blood cells from mature dogs contain less Na and more K than would be the case if they were in Donnan equilibrium with plasma. They have no ouabain-sensitive Na pump, and their membranes are deficient in Na, K-ATPase. Experiments are reported in which dog red cells were first loaded with supranormal quantities of Na and water and then reinjected into the dog. Over the course of 26–40 h the Na- and water-loaded cells returned to a normal state of hydration as judged by their density. It is concluded that dog red cells possess some means of correcting their swollen status in vivo, despite their lack of a ouabain-sensitive cation transport apparatus.

scholarly journals Normalizing effects of plasma on altered cation transport of red blood cells from essential hypertensive patients.

1983 ◽  
Vol 47 (12) ◽  
pp. 1387-1390 ◽  
Author(s):  
SHUNICHI KOJIMA ◽  
KEIICHI ITO ◽  
FUJIO DEGUCHI ◽  
TSUGUO OSADA ◽  
TERUNAO ASHIDA ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Cation Transport ◽  
Hypertensive Patients

Stomatocytosis Is Absent in “Stomatin”-Deficient Murine Red Blood Cells

Blood ◽  
1999 ◽  
Vol 93 (7) ◽  
pp. 2404-2410 ◽  
Author(s):  
Yiwen Zhu ◽  
Chris Paszty ◽  
Tikva Turetsky ◽  
Susan Tsai ◽  
Frans A. Kuypers ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Hemolytic Anemia ◽  
Blood Cells ◽  
Monovalent Cation ◽  
Hydration Status ◽  
Direct Role ◽  
Knock Out ◽  
Knock Out Mice ◽  
The Relationship

To examine the relationship between erythrocyte membrane protein 7.2b deficiency and the hemolytic anemia of human hereditary stomatocytosis, we created 7.2b knock-out mice by standard gene targeting approaches. Immunoblots showed that homozygous knock-out mice completely lacked erythrocyte protein 7.2b. Despite the absence of protein 7.2b, there was no hemolytic anemia and mouse red blood cells (RBCs) were normal in morphology, cell indices, hydration status, monovalent cation content, and ability to translocate lipids. The absence of the phenotype of hereditary stomatocytosis implies that protein 7.2b deficiency plays no direct role in the etiology of this disorder and casts doubt on the previously proposed role of this protein as a mediator of cation transport in RBC.

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