内皮:血管信息交换

R. Wei, S. Lunn, S. Gust, P. Kerr, F. Plane
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引用次数: 1

摘要

维持足够的血液流向组织和器官需要内皮细胞以刺激特异性的方式动态响应,以引起平滑肌收缩力的适当变化,从而引起动脉直径的适当变化。内皮细胞可直接受到血流量的增加和作用于表面受体的体液因子的刺激,也可通过血管周围神经释放的神经递质激活的平滑肌细胞的第二信使的通量受到刺激。内皮细胞对这些不同的输入产生刺激特异性反应的能力是由离子通道和信号蛋白组织到微结构域来促进的,这些微结构域允许微调的、空间限制的ca2 +事件来不同地激活关键效应物,如一氧化氮(NO)合成酶和ca2 +激活的K + (K Ca)通道。NO是一种扩散性介质,局部作用引起血管舒张。钾钙通道的打开引起内皮膜电位的超极化,并扩散到周围的平滑肌细胞,引起局部血管舒张。然而,一旦开始,超极化也通过内皮纵向扩散,影响多动脉段内血流的协调变化。因此,特定刺激激活的信号通路决定了它对动脉直径的影响是局部的还是可以影响血管床水平的血流。通过增加剪应力。剪切应力诱导的ca2 +通过内皮细胞管腔表面TRPV4通道内流导致信号微域内空间受限的ca2 +火花,选择性激活SK Ca通道和内皮NOS (eNOS)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Endothelium: The Vascular Information Exchange
Maintenance of adequate blood flow to tissues and organs requires that endothelial cells dynamically respond in a stimulus-specific manner to elicit appropriate changes in smooth muscle contractility and thus, arterial diameter. Endothelial cells can be stimu- lated directly by increases in blood flow and by humoral factors acting on surface receptors, as well as through flux of second messengers from smooth muscle cells activated by release of neurotransmitters from perivascular nerves. The ability of endothelial cells to generate stimulus-specific responses to these diverse inputs is facilitated by organization of ion channels and signaling proteins into microdomains that permit finely-tuned, spatially-restricted Ca 2+ events to differentially activate key effectors such as nitric oxide (NO) synthase and Ca 2+ -activated K + (K Ca ) channels. NO is a diffusible mediator which acts locally to cause vasodilation. Opening of K Ca channels causes hyperpolarization of the endothelial membrane potential which spreads to surrounding smooth muscle cells to also cause local vasodilation. However, once initiated, hyperpolarization also spreads longitudinally through the endothelium to effect coordinated changes in blood flow within multiple arterial segments. Thus, the signaling pathways activated by a particular stimulus determine whether it ’ s effects on arterial diameter are localized or can impact blood flow at the level of the vascular bed. by increases in shear stress. Shear stress-evoked Ca 2+ influx through TRPV4 channels on the luminal surface of endothelial cells leads to spatially-restricted Ca 2+ sparklets within a signaling microdomain to selectively activate SK ca channels and endothelial NOS (eNOS).
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