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首页> 外文期刊>American Journal of Physiology >Endothelial coordination of cerebral vasomotion via myoendothelial gap junctions containing connexins 37 and 40.
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Endothelial coordination of cerebral vasomotion via myoendothelial gap junctions containing connexins 37 and 40.

机译：通过含有连接蛋白37和40的心肌内皮间隙连接对大脑血管运动的内皮协调作用。

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摘要

Control of cerebral vasculature differs from that of systemic vessels outside the blood-brain barrier. The hypothesis that the endothelium modulates vasomotion via direct myoendothelial coupling was investigated in a small vessel of the cerebral circulation. In the primary branch of the rat basilar artery, membrane potential, diameter, and calcium dynamics associated with vasomotion were examined using selective inhibitors of endothelial function in intact and endothelium-denuded arteries. Vessel anatomy, protein, and mRNA expression were studied using conventional electron microscopy high-resolution ultrastructural and confocal immunohistochemistry and quantitative PCR. Membrane potential oscillations were present in both endothelial cells and smooth muscle cells (SMCs), and these preceded rhythmical contractions during which adjacent SMC intracellular calcium concentration ([Ca(2+)](i)) waves were synchronized. Endothelium removal abolished vasomotion and desynchronized adjacent smooth muscle cell [Ca(2+)](i) waves. N(G)-nitro-l-arginine methyl ester (10 microM) did not mimic this effect, and dibutyryl cGMP (300 muM) failed to resynchronize [Ca(2+)](i) waves in endothelium-denuded arteries. Combined charybdotoxin and apamin abolished vasomotion and depolarized and constricted vessels, even in absence of endothelium. Separately, (37,43)Gap27 and (40)Gap27 abolished vasomotion. Extensive myoendothelial gap junctions (3 per endothelial cell) composed of connexins 37 and 40 connected the endothelial cell and SMC layers. Synchronized vasomotion in rat basilar artery is endothelium dependent, with [Ca(2+)](i) waves generated within SMCs being coordinated by electrical coupling via myoendothelial gap junctions.
机译：对脑血管的控制不同于血脑屏障外部的系统性血管。在脑循环的一个小血管中研究了内皮通过直接的血管内皮偶联调节血管运动的假说。在大鼠基底动脉的初级分支中，使用选择性抑制剂在完整和内皮剥夺的动脉中检查膜电位，直径和与血管运动相关的钙动力学。使用常规电子显微镜高分辨率超微结构和共聚焦免疫组织化学和定量PCR研究了血管的解剖结构，蛋白质和mRNA的表达。内皮细胞和平滑肌细胞（SMCs）中都存在膜电位振荡，并且这些振荡发生在节律性收缩之前，在此过程中，相邻SMC细胞内钙浓度（[Ca（2 +）]（i））波同步。去除内皮细胞消除了血管运动，并使邻近的平滑肌细胞[Ca（2 +）]（i）波失去同步。 N（G）-硝基-1-精氨酸甲酯（10 microM）不能模拟这种效果，二丁酰cGMP（300μM）无法使内皮剥落的动脉中的[Ca（2 +）]（i）波重新同步。甚至在没有内皮细胞的情况下，混合使用的Charybdotoxin和Apamin可以消除血管运动，使血管去极化和收缩。 （37,43）Gap27和（40）Gap27分别取消了血管舒缩功能。由连接蛋白37和40组成的广泛的心肌内皮间隙连接（每个内皮细胞3个）连接内皮细胞和SMC层。大鼠基底动脉中的同步血管运动是内皮依赖性的，SMC中产生的[Ca（2 +）]（i）波通过经由肌内皮间隙连接的电耦合来协调。

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