Calcium permeability in deoxygenated sickle erythrocytes - abstract
West Indian med. j
; West Indian med. j;38(Suppl. 1): 66, April, 1989.
Article
en En
| MedCarib
| ID: med-5636
Biblioteca responsable:
JM3.1
Ubicación: JM3.1; R18.W4
ABSTRACT
Sickle cell have an abnormally high level of calcium and, by an unknown mechanism, exhibit an increase in Caý+ permeability when they are sickled upon deoxygenation. This reversible increase in Caý+ permeability might contribute to cell dehydration by activation of K+ and water loss through the Caý+ permeability might contribute to cell dehydration by activation of K+ and water loss through the Caý+ dependent K+ channel (Gardos pathway). In the present study, the mechanism involved in Ca+ influx stimulation in sickle cells induced by deoxygenation was investigated by three different experiments Ca2+uptake (1) in the presence of an extracellular impermeant marker to test endocytosis, (2) in the presence of the Caý+uptake (1) in the presence of an extracellular impermeant marker to test endocytosis, (2) in the presence of the Caý= -channel inhibitor Nifedipine, and (3) in the presence of an anion-exchanger inhibitor 4,4' - diisothiocyanatostilbene-2,2' - disulfonic acid (DIDS). These experiments revealed that endocytosis accounted for 6 percent to 19 percent of the Ca2+ uptake in deoxygenated sickle cells a nd that the increased Ca2+ influx was in part blocked by Nifedipine and by DIDS. The present findings, describing different pathways involved in the Caý+ increased permeability of deoxygenated sickle cells are of potential therapeutic interest (AU)
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Colección:
01-internacional
Base de datos:
MedCarib
Asunto principal:
Calcio
/
Eritrocitos
/
Anemia de Células Falciformes
Idioma:
En
Revista:
West Indian med. j
Año:
1989
Tipo del documento:
Article
/
Congress and conference