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在鼠胃窦平滑肌细胞中,低电压激活内向电流是一种假象。

Low-voltage-activated inward current in murine antral smooth muscle cells is an artifact.

机构信息

Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada.

出版信息

Am J Physiol Cell Physiol. 2021 Jun 1;320(6):C966-C973. doi: 10.1152/ajpcell.00031.2021. Epub 2021 Mar 31.

DOI:10.1152/ajpcell.00031.2021
PMID:33788632
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8285640/
Abstract

Two types of voltage-dependent inward currents were evoked by depolarization in murine antral smooth muscle cells (SMCs) bathed in Ca-containing physiological solution: high-voltage-activated (HVA) and low-voltage-activated (LVA) inward currents. We examined whether the LVA current was due to: ) T-type Ca channels, ) Ca-activated Clchannels, ) nonselective cation channels (NSCC), or ) voltage-dependent K channels. Replacement of external Ca (2 mM) with equimolar Ba increased the amplitude of the HVA current but blocked the LVA current. Nicardipine blocked the HVA current, and in the presence of nicardipine, T-type Ca blockers failed to block LVA current. A Cl channel antagonist had little effect on LVA current. Cation-free external solution completely abolished both HVA and LVA currents. Addition of Ca to the solution restored only HVA currents. Addition of K (5 mM) to otherwise cation-free solution induced LVA current that reversed at -20 mV. These data suggest that LVA current is not due to T-type Ca channels, Ca-activated Cl channels, or NSCC. A-type K (K) currents and delayed rectifying K (K) currents can be resolved in antral SMCs dialyzed with a solution containing 140 mM K. When cells were exposed to high K external solution and dialyzed with Cs-rich solution in the presence of nicardipine, LVA current was evoked and reversed at positive potentials. LVA currents were blocked by K channel blockers, 4-aminopyridine, and tetraethylammonium. In conclusion, LVA inward currents can be generated by K influx via K channels in murine antral SMCs when cells were dialyzed with Cs-rich solution.

摘要

两种电压依赖性内向电流可在含有 Ca2+的生理溶液中被去极化激活:高电压激活(HVA)和低电压激活(LVA)内向电流。我们检测了 LVA 电流是否是由于:)T 型 Ca 通道;)Ca 激活的 Cl 通道;)非选择性阳离子通道(NSCC);或)电压依赖性 K 通道。用等摩尔 Ba 取代外 Ca(2 mM)增加了 HVA 电流的幅度,但阻断了 LVA 电流。尼卡地平阻断了 HVA 电流,而在尼卡地平存在的情况下,T 型 Ca 通道阻滞剂未能阻断 LVA 电流。Cl 通道拮抗剂对 LVA 电流几乎没有影响。无阳离子的外液完全消除了 HVA 和 LVA 电流。向溶液中添加 Ca 仅恢复了 HVA 电流。向无阳离子的溶液中添加 K(5 mM)诱导出 LVA 电流,其在-20 mV 处反转。这些数据表明 LVA 电流不是由于 T 型 Ca 通道、Ca 激活的 Cl 通道或 NSCC 引起的。A 型 K(K)电流和延迟整流 K(K)电流可在用含有 140 mM K 的溶液透析的胃窦平滑肌细胞中得到区分。当细胞暴露于高 K 外液并在尼卡地平存在下用富含 Cs 的溶液透析时,会诱发并在正电位处反转 LVA 电流。LVA 电流被 K 通道阻滞剂 4-氨基吡啶和四乙铵阻断。总之,当用富含 Cs 的溶液透析时,胃窦平滑肌细胞中的 K 流入可通过 K 通道产生 LVA 内向电流。

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