ULTRASTRUCTURAL-LOCALIZATION OF CHOLINE ACETYLTRANSFERASE IN VASCULAR ENDOTHELIAL-CELLS IN RAT-BRAIN
ULTRASTRUCTURAL-LOCALIZATION OF CHOLINE ACETYLTRANSFERASE IN VASCULAR ENDOTHELIAL-CELLS IN RAT-BRAIN
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DOI：
10.1038/316724a0
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发表时间：
1985-01-01
期刊：
影响因子：
64.8
通讯作者：
BURNSTOCK, G
中科院分区：
文献类型：
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作者：
PARNAVELAS, JG;KELLY, W;BURNSTOCK, G
Furchgot和Zawadski已经证明，乙酰胆碱(ACh)不直接作用于血管壁的平滑肌肉，而是通过管腔内皮细胞上的受体释放内皮衍生的松弛因子(EDRF)。由于动脉周围神经释放的神经递质不太可能在作用于内皮细胞释放EDRF以产生血管扩张之前通过内侧肌衣扩散至中膜，这一发现被认为是一种病理生理机制的迹象，而不是生理机制(见参考文献2，3)。ACh在血液中被乙酰胆碱酯酶迅速降解，因此ACh必须在局部释放才能对内皮细胞有效。在这里，我们证明了胆碱乙酰转移酶在小脑血管内皮细胞中的免疫细胞化学定位，这与ACh起源于内皮细胞的观点是一致的，内皮细胞可以合成和储存它。我们认为，在缺血损伤内皮细胞后ACh的释放参与了血管扩张的病理生理机制，该机制保护该段血管免受进一步损伤，并保护脑细胞免受缺氧的影响。
Furchgott and Zawadski1have shown that acetylcholine (ACh) does not act directly on the smooth muscle of blood vessel walls, but rather via receptors on the endothelial cells lining the lumen, to release an endothelium-derived relaxing factor (EDRF). As it is very unlikely that neurotransmitter released from the periarterial nerves, which are confined to the adventitial–medial border, diffuses all the way through the medial muscle coat before acting on endothelial cells to release EDRF to produce vasodilatation, this discovery has been regarded as an indication of a pathophysiological mechanism, rather than a physiological one (see refs 2,3). ACh is rapidly degraded in the blood by acetylcholinesterase, so that ACh must be released locally to be effective on endothelial cells. Here we demonstrate the immunocytochemical localization of choline acetyltransferase in endothelial cells of small brain vessels, which is consistent with the view that the ACh originates from endothelial cells that can synthesize and store it. We suggest that release of ACh following damage to endothelial cells during ischaemia contributes to a pathophysiological mechanism of vasodilation which protects that segment of vessel from further damage as well as brain cells from hypoxia.