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Intracellularly regulated Ca2+ influx or remnants of extracellularly activated signalling pathway in human red blood cells?
Lakatoš, Boris, Hudec, Roman and Varečka, Ľudovít Intracellularly regulated Ca2+ influx or remnants of extracellularly activated signalling pathway in human red blood cells? Acta Chimica Slovaca, Vol.1, No. 1, 2008, 180-191
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Attached Files |
Name |
Description |
MIMEType |
Size |
Downloads |
acs_0017.pdf
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acs_0017.pdf |
application/pdf |
373.13KB |
0 |
Author(s) |
Lakatoš, Boris Hudec, Roman Varečka, Ľudovít
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Title |
Intracellularly regulated Ca2+ influx or remnants of extracellularly activated signalling pathway in human red blood cells?
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Journal name |
Acta Chimica Slovaca
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Publication date |
2008
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Year available |
2008
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Volume number |
1
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Issue number |
1
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ISBN |
978-80-227-2957-4
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Start page |
180
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End page |
191
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Total pages |
12
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Place of publication |
Bratislava
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Publisher |
Slovak Technical University
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Collection year |
2008
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Language |
english
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Subject |
270000 Biological Sciences 270100 Biochemistry and Cell Biology 270300 Microbiology
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Abstract/Summary |
Phorbol-14-myristate-13-acetate (PMA) (10-7-10-6 mol/l) inhibited the Ca2+-dependent K+ efflux (the Gárdos effect - GE) induced by Ca2+, the hyperpolarisation accompanying the GE, the vanadate-induced 45Ca2+ influx, and depolarised the membrane, in vanadate-treated human red blood cells (RBC). The GE induced by propranolol (PLL) was not inhibited by PMA. Both PMA and PLL stimulated the basal 45Ca2+ influx. These results suggest that a) protein kinase C activity prevents the activation of GE by vanadate but PLL bypasses this mechanism, b) the stimulation of the Ca2+ influx by PMA and the GE inhibition are caused by the membrane depolarisation, c) the basal Ca2+ influx in human RBC is regulated in a complex manner, and d) the effect of vanadate resembles to the activation of agonist-stimulated signalling pathway in non-excitable cells.
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Keyword(s) |
Human red blood cells Ca2+ influx Gárdos effect Ca2+-activated K+ channel propranolol vanadate PMA
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