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Ion channel mechanism of regulatory volume decrease in human epithelial cells / 中国应用生理学杂志
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-252769
Biblioteca responsável: WPRO
ABSTRACT
<p><b>AIM</b>To observe the regulatory volume decrease (RVD) process of human intestine cells and investigate its ion channel mechanism.</p><p><b>METHODS</b>Cultured human intestine cells were exposed to hypotonic solution and the cell volume was measured using Coulter Counter System. RT-PCR was explored to detect the mRNA expression of Ca(2+) -activated K+ channel.</p><p><b>RESULTS</b>Human intestine cells showed a RVD process and this process could be blocked by Cl- channel blocker NPPB and K+ channel blocker TEA. Further results demonstrated the subtype of K+ channel involved in RVD was an intermediate-conductance, Ca(2+) -activated K+ channel (IK) because of its high sensitivity to clotrimazole. RT-PCR results also showed the expression of IK in this cell line.</p><p><b>CONCLUSION</b>The RVD process of intestine cell was dependent on the parallel activation of Cl- channel and K+ channel. The subtype of K+ channel in volved in the RVD process was IK channel.</p>
Assuntos
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Assunto principal: Farmacologia / Canais de Potássio / Linhagem Celular / Canais de Cloreto / Biologia Celular / Canais de Potássio Cálcio-Ativados / Bloqueadores dos Canais de Potássio / Tamanho Celular / Células Epiteliais / Soluções Hipotônicas Limite: Humanos Idioma: Chinês Revista: Chinese Journal of Applied Physiology Ano de publicação: 2008 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Assunto principal: Farmacologia / Canais de Potássio / Linhagem Celular / Canais de Cloreto / Biologia Celular / Canais de Potássio Cálcio-Ativados / Bloqueadores dos Canais de Potássio / Tamanho Celular / Células Epiteliais / Soluções Hipotônicas Limite: Humanos Idioma: Chinês Revista: Chinese Journal of Applied Physiology Ano de publicação: 2008 Tipo de documento: Artigo
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