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首页> 外文期刊>Journal of vascular research >alpha2-Adrenoceptor activation increases calcium channel currents in single vascular smooth muscle cells isolated from human omental resistance arteries.
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alpha2-Adrenoceptor activation increases calcium channel currents in single vascular smooth muscle cells isolated from human omental resistance arteries.

机译:alpha2-肾上腺素受体激活增加了从人网膜阻力动脉分离的单个血管平滑肌细胞中的钙通道电流。

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摘要

Single cells were freshly isolated from human omental resistance arteries using an enzymatic dispersion technique. Calcium channel currents (IBa) were recorded using whole cell voltage clamp techniques with Ba2+ as the charge carrier. BHT 933, a selective alpha2-adrenoceptor agonist, increased IBa. The effect of BHT 933 was reversible following washout. The action of BHT 933 was blocked by yohimbine. Pretreatment of tissues with pertussis toxin for 18 h or inclusion of GDP-beta-S in the intracellular patch pipette solution also prevented the BHT 933-induced rise in IBa, but had no effect on IBa in the absence of BHT 933. Activation of alpha2-adrenoceptors in human vascular smooth muscle cells increases IBa by a mechanism involving a pertussis toxin-sensitive G protein.
机译:使用酶分散技术从人网膜阻力动脉新鲜分离单细胞。使用全电池电压钳制技术(以Ba2 +作为电荷载体)记录钙通道电流(IBa)。选择性α2-肾上腺素受体激动剂BHT 933增加了IBa。冲洗后,BHT 933的作用是可逆的。 BHT 933的作用被育亨宾所阻止。用百日咳毒素预处理组织18 h或在细胞内贴片吸管溶液中加入GDP-β-S还可防止BHT 933诱导的IBa升高,但在不存在BHT 933的情况下对IBa无效。alpha2的激活人血管平滑肌细胞中的β-肾上腺素受体通过涉及百日咳毒素敏感的G蛋白的机制增加IBa。

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