Differential Changes of ATP-sensitive Potassium Channel Current after Hypoxia-reperfusion Treatment in Mouse Neuroblastoma 2a (N2a) Cell
The Korean Journal of Physiology and Pharmacology
;
: 183-186, 2002.
Artigo
em Inglês
| WPRIM
| ID: wpr-728053
ABSTRACT
Ischemic damage is one of the most serious problems. The openers of KATP channel have been suggested to have an effect to limit the ischemic damage. However, it is not yet clear how KATP channels of a cell correspond to hypoxic damage. To address the question, N2a cells were exposed to two different hypoxic conditions as follows 6 hours hypoxia followed by 3 hours reperfusion and 12 hours hypoxia followed by 3 hours reperfusion. As the results, 6 hours hypoxic treatment increased glibenclamide-sensitive basal KATP current activity (approximately 6.5-fold at 0 mV test potential) when compared with nomoxic condition. In contrast, 12 hours hypoxic treatment induced a relatively smaller change in the KATP current density (2.5-fold at 0 mV test potential). Additionally, in experiments where KATP channels were opened using diazoxide, the hypoxia for 6 hours significantly increased the current density in comparison to control condition (p < 0.001). Interestingly, the augmentation in the KATP current density reduced after exposure to the 12 hours hypoxic condition (p < 0.001). Taken together, these results suggest that KATP channels appear to be recruited more in cells exposed to the 6 hours hypoxic condition and they may play a protective role against hypoxia-reperfusion damage within the time range.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Potássio
/
Canais de Potássio
/
Reperfusão
/
Glibureto
/
Diazóxido
/
Canais KATP
/
Hipóxia
/
Neuroblastoma
Tipo de estudo:
Estudo diagnóstico
Limite:
Animais
Idioma:
Inglês
Revista:
The Korean Journal of Physiology and Pharmacology
Ano de publicação:
2002
Tipo de documento:
Artigo
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