Electromagnetic energy (670 nm) stimulates vasodilation through activation of the large conductance potassium channel (BKCa).

Electromagnetic energy (670 nm) stimulates vasodilation through activation of the large conductance potassium channel (BKCa).
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DOI:
10.1371/journal.pone.0257896
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发表时间:
2021
期刊:
影响因子:
3.7
通讯作者:
Lohr NL
Lohr NL
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Gebremendhin D;Lindemer B;Weihrauch D;Harder DR;Lohr NL

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外周动脉疾病(PAD)是一种高度病态的疾病,在这种疾病中,流向四肢的血液受损会导致疼痛和组织丧失。之前我们发现670纳米电磁能量(R/NIR)可以增加细胞和组织中的一氧化氮水平。一氧化氮通过刺激钾外排和膜超极化引起平滑肌(SMC)松弛。能量对离子通道活性的作用还有待探索。在这里,我们假设R/NIR通过激活SMC中的钾通道刺激血管舒张。分离C57Bl/6和Slo1-/-小鼠的股动脉或面动脉,加压至60 mmHg,用U46619预缩,用能量R/NIR (10 mW/cm2,持续5分钟)照射两次,两次照射之间有10分钟的暗期。利用膜片钳技术,在室温下记录新分离的小鼠股动脉肌细胞附着和切除的内外膜贴片上的单通道K+电流。R/NIR刺激的血管舒张需要大电导钾通道的功能性激活。在光刺激下,SMC中存在电压依赖的向外电流,这是由于通道打开的打开状态概率增加。通道打开的R/NIR调节在药理学上(paxilline)和遗传学上(BKca α亚基敲除)被消除。光没有直接作用来调节通道活动,因为切除的斑块并没有增加通道打开的开放状态概率。R/NIR血管舒张需要间接激活BKca通道。
Peripheral artery disease (PAD) is a highly morbid condition in which impaired blood flow to the limbs leads to pain and tissue loss. Previously we identified 670 nm electromagnetic energy (R/NIR) to increase nitric oxide levels in cells and tissue. NO elicits relaxation of smooth muscle (SMC) by stimulating potassium efflux and membrane hyperpolarization. The actions of energy on ion channel activity have yet to be explored. Here we hypothesized R/NIR stimulates vasodilation through activation of potassium channels in SMC. Femoral arteries or facial arteries from C57Bl/6 and Slo1-/- mice were isolated, pressurized to 60 mmHg, pre-constricted with U46619, and irradiated twice with energy R/NIR (10 mW/cm2 for 5 min) with a 10 min dark period between irradiations. Single-channel K+ currents were recorded at room temperature from cell-attached and excised inside-out membrane patches of freshly isolated mouse femoral arterial muscle cells using the patch-clamp technique. R/NIR stimulated vasodilation requires functional activation of the large conductance potassium channels. There is a voltage dependent outward current in SMC with light stimulation, which is due to increases in the open state probability of channel opening. R/NIR modulation of channel opening is eliminated pharmacologically (paxilline) and genetically (BKca α subunit knockout). There is no direct action of light to modulate channel activity as excised patches did not increase the open state probability of channel opening. R/NIR vasodilation requires indirect activation of the BKca channel.
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