首页> 外文期刊>American Journal of Physiology >Chronic carbon monoxide enhanced IbTx-sensitive currents in rat resistance pulmonary artery smooth muscle cells.
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Chronic carbon monoxide enhanced IbTx-sensitive currents in rat resistance pulmonary artery smooth muscle cells.

机译:慢性一氧化碳增强了大鼠抵抗性肺动脉平滑肌细胞中的IbTx敏感电流。

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摘要

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.
机译:外源性一氧化碳(CO)可直接作用于肺动脉(PA)平滑肌细胞,从而诱导肺血管舒张。我们调查了K +通道对对照(PAC)大鼠和以530份/百万的CO暴露3 wk的大鼠(称为PACO大鼠)的抗PA静息膜电位调节的贡献。全细胞膜片钳实验表明,PACO细胞的静息膜电位比PAC细胞的负膜电位更负。这与PACO细胞膜抗性的降低有关。进一步的分析表明,PACO细胞的向外电流密度高于PAC细胞(+60 mV时为50%)。这与对纤毛毒素(IbTx)敏感的电流增加有关。加压PA的慢性CO超极化膜从-46.9 +/- 1.2到-56.4 +/- 2.6 mV。另外,IbTx使PACO动脉的平滑肌细胞膜显着去极化,而PAC动脉则没有。本研究提供了暴露于慢性CO的大鼠PA的平滑肌细胞中Ca2 +激活的K +电流增加的初步证据。

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