Inhibitory effect of ethanol on voltage-dependent potassium currents in single aortic smooth muscle cells.

S. -. Wu, C. Chao
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引用次数: 6

Abstract

The effect of ethanol on voltage-dependent K+ currents was examined in single aortic smooth muscle cells. The aortic smooth muscle cells were isolated from guinea pigs. The tight-seal patch clamp technique in whole cell configuration was employed. Ethanol (500 mM) reversibly inhibited voltage-dependent transient outward K+ current, the spontaneous transient oscillatory K+ current (STOC) and steady-state K+ current, whereas ethanol (50 mM) did not produce any change in these K+ currents. When the peak-height amplitudes of STOC were analyzed, the application of ethanol (50 mM) was noted to produce significant inhibition on both amplitude and frequency of STOC evoked at the holding potential of +10 mV. The results shown in the present study indicate that ethanol-induced inhibition of the voltage-dependent K+ channel, which is not required for the elicitation of either GTP-binding protein(s) or inositol triphosphate, may contribute to its vasoconstrictor effect because the inhibition of the voltage-dependent K+ channel may lead to the increase of cell excitability in vascular smooth muscle.
乙醇对单个主动脉平滑肌细胞电压依赖性钾电流的抑制作用。
在单个主动脉平滑肌细胞中检测了乙醇对电压依赖性K+电流的影响。从豚鼠身上分离主动脉平滑肌细胞。采用全细胞形态膜片钳紧封技术。500mm乙醇可逆抑制电压依赖性瞬态外向K+电流、自发瞬态振荡K+电流(STOC)和稳态K+电流,而50mm乙醇对这些K+电流没有任何影响。当分析STOC的峰高振幅时,我们注意到乙醇(50 mM)的应用对+10 mV保持电位下诱发的STOC的振幅和频率都有显著的抑制作用。本研究的结果表明,乙醇诱导的电压依赖性K+通道的抑制可能有助于其血管收缩作用,因为电压依赖性K+通道的抑制可能导致血管平滑肌细胞兴奋性的增加,而gtp结合蛋白或肌醇三磷酸的激发都不需要这种抑制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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