Properties of acetylcholine-induced hyperpolarization in smooth muscle cells of the mouse mesenteric artery
Properties of acetylcholine-induced hyperpolarization in smooth muscle cells of the mouse mesenteric artery
复制标题
DOI：
10.1540/jsmr.43.219
复制
发表时间：
2007-12-01
影响因子：
--
通讯作者：
Suzuki, Hikaru
中科院分区：
文献类型：
--
作者：
Koshita, Makoto;Hidaka, Kiyoshi;Suzuki, Hikaru
本文观察了乙酰胆碱（ACh）引起的小鼠肠系膜动脉平滑肌细胞超极化特性。平滑肌细胞的静息膜电位约为-60 mV。当ACh（10 μ M）施加1分钟时，膜超极化，在约1分钟内达到约5 mV的峰值幅度，随后在从灌流液（恢复组分）中撤出ACh后，电位在约7分钟内缓慢恢复到静息水平。动脉暴露于0.5 mM Ba 2+（一种内向整流K通道抑制剂），使膜去极化约13 mV，使ACh诱导的超极化幅度增加至约10 mV，并促进恢复组分的可视化。吲哚美辛（10 μ M），环氧合酶的抑制剂，抑制了恢复组件，并因此减少了超极化的持续时间。乙酰胆碱诱导的反应没有显着改变，无论是N-ω-硝基-L-精氨酸（10 μ M），一氧化氮（NO）生产的抑制剂，或过氧化氢酶（130 U/ml），超氧化物清除剂。外源施加过氧化氢（H2 O2，300 μ M）超极化膜约5 mV，这是废除过氧化氢酶。这些结果表明，在小鼠肠系膜动脉，乙酰胆碱诱导的超极化有两个组成部分，吲哚美辛敏感和吲哚美辛不敏感的组件。前一种成分可能由前列腺素类产生，而后者可能由NO或H2 O2以外的因素产生。结果还表明，内向整流钾通道可能是产生静息膜电位的重要通道，但可能不是乙酰胆碱诱导的小鼠肠系膜动脉平滑肌细胞膜超极化的主要原因。
The properties of smooth muscle cell hyperpolarization produced by acetylcholine (ACh) were investigated in mesenteric arteries isolated from mice. The resting membrane potential of the smooth muscle cells was about -60 mV. When ACh (10 mu M) was applied for 1 min, the membrane hyperpolarized with a peak amplitude of about 5 mV which was reached in about 1 min, following which the potential slowly reverted to the resting level over about 7 min following withdrawal of ACh from the superfusate (recovery component). Exposure of the artery to 0.5 mM Ba2+, an inhibitor of inward rectifier K-channels, depolarized the membrane by about 13 mV, increased the amplitude of the ACh-induced hyperpolarization to about 10 mV, and facilitated the visualization of the recovery component. Indomethacine (10 mu M), an inhibitor of cyclooxygenase, inhibited the recovery component and as a consequence reduced the duration of the hyperpolarization. The ACh-induced response was not markedly altered by either N-omega-nitro-L-arginine (10 mu M), an inhibitor of nitric oxide (NO) production, or catalase (130 U/ml), a super oxide scavenger. Exogenously applied hydrogen peroxide (H2O2, 300 mu M) hyperpolarized the membrane by about 5 mV, which was abolished by catalase. These results suggest that in the mouse mesenteric artery, the ACh-induced hyperpolarization has two components, both an indomethacin-sensitive and an indomethacin-insensitive component. The former component may be produced by prostanoids, while the latter may be produced by factors other than NO or H2O2. The results also suggested that the inward rectifier K-channels may be important for producing the resting membrane potential, but they may not be the main contributor to the ACh-induced hyperpolarization of smooth muscle cell membranes in the mouse mesenteric artery.