Innervation of the human middle meningeal artery:: Immunohistochemistry, ultrastructure, and role of endothelium for vasomotility

Innervation of the human middle meningeal artery:: Immunohistochemistry, ultrastructure, and role of endothelium for vasomotility
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DOI:
10.1016/s0196-9781(98)00066-7
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发表时间:
1998-01-01
期刊:
影响因子:
3
通讯作者:
Jansen-Olesen, I
Jansen-Olesen, I
中科院分区:
医学3区
文献类型:
--
作者:
Edvinsson, L;Gulbenkian, S;Jansen-Olesen, I

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脑膜中动脉和分支小动脉中的大多数神经纤维是交感神经,储存去甲肾上腺素和神经肽Y(NPY)。稀疏的纤维供应含有乙酰胆碱酯酶活性和对血管活性肠肽(VIP)、肽组氨酸蛋氨酸(PHM)和降钙素基因相关肽(CGRP)的免疫反应性。只有少数P物质和神经肽K免疫反应阳性纤维。电子显微镜显示轴突和终末位于人脑膜中动脉的外膜内侧边缘,与平滑肌细胞的距离相当大(>500 nM)。几个轴突配置文件包含不同类型的囊泡,包括推定的感觉配置文件。血管周围储存的信号物质去甲肾上腺素和NPY可引起血管收缩。乙酰胆碱和P物质引起的舒张,这些显着减少,在动脉无内皮,而反应去甲肾上腺素,NPY,VIP,PHM,和CORP内皮去除没有改变。阻断实验表明,哌唑嗪阻断了血管对去甲肾上腺素的反应,BLBP 3226阻断了血管对NPY的反应,阿托品阻断了血管对乙酰胆碱的反应,RP 67580阻断了血管对P物质的反应,人α-CGRP阻断了血管对人α-CGRP的反应(8-37)。(C)1998年爱思唯尔科学公司
The majority of nerve fibers in the middle meningeal artery and branching arterioles are sympathetic, storing norepinephrine and neuropeptide Y (NPY). A sparse supply of fibers contain acetylcholinesterase activity and immunoreactivity toward vasoactive intestinal peptide (VIP), peptidine histidine methionine (PHM), and calcitonin gene-related peptide (CGRP). Only few substance P and neuropeptide K immunoreactive fibers are noted. Electronmicroscopy shows axons and terminals at the adventitial medial border of the human middle meningeal artery, with a fairly large distance to the smooth muscle cells (>500 nM). Several axon profiles contain vesicles of different types, including putative sensory profiles. The perivascularly stored signal substances, norepinephrine and NPY induced vasoconstrictor. Relaxations were induced by acetylcholine and substance P, and these were significantly reduced in arteries without endothelium, while the responses to norepinephrine, NPY, VIP, PHM, and CORP were not changed by endothelium removal. Blockade experiments showed that the vasomotor responses to norepinephrine were blocked by prazosin, to NPY by BLBP 3226, acetylcholine by atropin, substance P by RP 67580, and the human alpha-CGRP response by human alpha-CGRP(8-37). (C) 1998 Elsevier Science Inc.