Chronic carbon monoxide enhanced IbTx-sensitive currents in rat resistance pulmonary artery smooth muscle cells
Chronic carbon monoxide enhanced IbTx-sensitive currents in rat resistance pulmonary artery smooth muscle cells
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DOI：
10.1152/ajplung.00004.2002
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发表时间：
2002-07-01
影响因子：
4.9
通讯作者：
Vandier, C
中科院分区：
文献类型：
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作者：
Dubuis, E;Gautier, M;Vandier, C
外源性一氧化碳(CO)可通过直接作用于肺动脉(PA)平滑肌细胞而诱导肺血管扩张。我们观察了K+通道对正常大鼠(PAC)和CO染毒3wk(标记为PaCO大鼠)阻力PA静息膜电位的调节作用。全细胞膜片钳实验显示，PACO细胞的静息膜电位比PAC细胞的膜电位更负。这与PACO细胞膜阻力降低有关。进一步分析表明，PACO细胞的外向电流密度(+60 mV时为50%)高于PAC细胞。这与IBERIO毒素(IbTx)敏感电流的增加有关。加压PA慢性CO超极化从-46.9+/-1.2 mV到-56.4+/-2.6 mV。此外，IbTx对PaCO动脉的平滑肌细胞膜有明显的去极化作用，但对PAC动脉的去极化作用不明显。本研究为慢性一氧化碳暴露大鼠肺动脉平滑肌细胞钙激活钾电流的增加提供了初步证据。
Exogenous carbon monoxide (CO) can induce pulmonary vasodilation by acting directly on pulmonary artery (PA) smooth muscle cells. We investigated the contribution of K+ channels to the regulation of resistance PA resting membrane potential on control (PAC) rats and rats exposed to CO for 3 wk at 530 parts/ million, labeled as PACO rats. Whole cell patch-clamp experiments revealed that the resting membrane potential of PACO cells was more negative than that of PAC cells. This was associated with a decrease of membrane resistance in PACO cells. Additional analysis showed that outward current density in PACO cells was higher (50% at +60 mV) than in PAC cells. This was linked to an increase of iberiotoxin (IbTx)-sensitive current. Chronic CO hyperpolarized membrane of pressurized PA from -46.9 +/- 1.2 to -56.4 +/- 2.6 mV. Additionally, IbTx significantly depolarized membrane of smooth muscle cells from PACO arteries but not from PAC arteries. The present study provides initial evidence of an increase of Ca2+-activated K+ current in smooth muscle cells from PA of rats exposed to chronic CO.