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首页> 外文期刊>American Journal of Physiology >Hypoxia sensitivity of a voltage-gated potassium current in porcine intrapulmonary vein smooth muscle cells
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Hypoxia sensitivity of a voltage-gated potassium current in porcine intrapulmonary vein smooth muscle cells

机译：猪肺内静脉平滑肌细胞中电压门控钾电流的缺氧敏感性

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Hypoxia contracts the pulmonary vein, but the underlying cellular effectors remain unclear. Utilizing contractile studies and whole cell patch-clamp electrophysiology, we report for the first time a hypoxia-sensitive K + current in porcine pulmonary vein smooth muscle cells (PVSMC). Hypoxia induced a transient contractile response that was 56 ± 7% of the control response (80 mM KCl). This contraction required extracellular Ca 2+ and was sensitive to Ca 2+ channel blockade. Blockade of K + channels by tetraethylammonium chloride (TEA) or 4-aminopyridine (4-AP) reversibly inhibited the hypoxia-mediated contraction. Singleisolated PVSMC (typically 159.1 ± 2.3 μm long) had mean resting membrane potentials (RMP) of -36 ± 4 mV with a mean membrane capacitance of 108 ± 3.5 pF. Whole cell patch-clamp recordings identified a rapidly activating, partially inactivating K + current (IKH) that was hypoxia, TEA, and 4-AP sensitive. IKH was insensitive to Penitrem A or glyburide in PVSMC and had a time to peak of 14.4 ± 3.3 ms and recovered in 67 ms following inactivation at +80 mV. Peak window current was -32 mV, suggesting that I KH may contribute to PVSMC RMP. The molecular identity of the potassium channel is not clear. However, RT-PCR, using porcine pulmonary artery and vein samples, identified Kv 1.5, Kv 2.1, and BK, with all three being more abundant in the PV. Both artery and vein expressed STREX, a highly conserved and hypoxia-sensitive BK channel variant. Taken together, our data support the hypothesis that hypoxic inhibition of IKH would contribute to hypoxic-induced contraction in PVSMC.
机译：缺氧使肺静脉收缩，但潜在的细胞效应子仍不清楚。利用收缩性研究和全细胞膜片钳电生理学，我们首次报道了猪肺静脉平滑肌细胞（PVSMC）的低氧敏感性K +电流。低氧引起的短暂收缩反应为对照反应（80 mM KCl）的56±7％。该收缩需要细胞外Ca 2+，并且对Ca 2+通道阻滞敏感。四乙基氯化铵（TEA）或4-氨基吡啶（4-AP）阻断K +通道可逆地抑制了缺氧介导的收缩。单隔离PVSMC（通常长159.1±2.3μm）具有-36±4 mV的平均静息膜电位（RMP），平均膜电容为108±3.5 pF。全细胞膜片钳记录确定了对缺氧，TEA和4-AP敏感的快速激活，部分灭活的K +电流（IKH）。 IKH对PVSMC中的Penitrem A或格列本脲不敏感，峰值时间为14.4±3.3 ms，在+80 mV灭活后67 ms即可恢复。峰值窗口电流为-32 mV，表明I KH可能有助于PVSMC RMP。钾通道的分子身份尚不清楚。然而，使用猪肺动脉和静脉样本的RT-PCR可以鉴定出Kv 1.5，Kv 2.1和BK，这三个都在PV中更为丰富。动脉和静脉都表达STREX，这是高度保守且对缺氧敏感的BK通道变异。综上所述，我们的数据支持以下假设：IKH的低氧抑制将导致低氧诱导的PVSMC收缩。

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