Dux Maria, Sántha Péter, Jancsó Gabor
Department of Physiology, University of Szeged, Dóm tér 10, H-6720 Szeged, Hungary.
J Physiol. 2003 Nov 1;552(Pt 3):859-67. doi: 10.1113/jphysiol.2003.050633. Epub 2003 Aug 29.
The neurogenic sensory vascular responses of the dura mater encephali are considered to contribute significantly to the mechanisms of meningeal nociception and headache. Although the fundamental role of capsaicin-sensitive afferent nerves in the development of the neurogenic inflammatory responses of a variety of tissues is well established, their participation in meningeal vascular reactions is unclear. In the present study, the effects of the topical application of capsaicin on the dural blood flow and on the morphology of the dural nerve fibres were examined in control and capsaicin-pretreated rats by means of laser Doppler flowmetry and electron microscopy, respectively. In the control rats, the dural application of capsaicin at concentrations of 50 and 100 nM induced significant increases in blood flow in the branches of the medial meningeal artery. This capsaicin-induced vasodilatation was abolished by capsazepine, a transient receptor potential vanilloid 1 (TRPV1) receptor antagonist, and by hCGRP8-37, a calcitonin gene-related peptide (CGRP) receptor antagonist. Administration of capsaicin at higher concentrations (1 and 10 microM) resulted in marked, dose-dependent decreases in dural blood flow. The capsaicin-induced vasodilatation was abolished, whereas vasoconstriction was augmented, by systemic pretreatment of the animals with capsaicin. Electron microscopy revealed degenerating unmyelinated axons in the dura mater after an acute exposure to capsaicin (10 microM), providing support for the existence and possible functional role of capsaicin-sensitive dural afferent nerves. The results indicate that capsaicin-induced vasodilatation in the rat dura mater is mediated by the release of CGRP from the sensory nerves, whereas the vasoconstrictor response may be attributed to a direct action of capsaicin on the vascular smooth muscle. The present study demonstrates for the first time that capsaicin-sensitive nociceptive afferent nerves contribute significantly to the dural vasodilatory responses and suggests an important role in meningeal nociception.
硬脑膜的神经源性感觉血管反应被认为在脑膜伤害感受和头痛机制中起重要作用。尽管辣椒素敏感传入神经在多种组织的神经源性炎症反应发展中的基本作用已得到充分证实,但其在脑膜血管反应中的参与情况尚不清楚。在本研究中,分别通过激光多普勒血流仪和电子显微镜,检测了辣椒素局部应用对对照大鼠和经辣椒素预处理大鼠的硬脑膜血流及硬脑膜神经纤维形态的影响。在对照大鼠中,50和100 nM浓度的辣椒素硬膜内应用可引起脑膜中动脉分支血流显著增加。这种辣椒素诱导的血管舒张被辣椒素受体拮抗剂capsazepine和降钙素基因相关肽(CGRP)受体拮抗剂hCGRP8 - 37消除。更高浓度(1和10 μM)的辣椒素给药导致硬脑膜血流显著的剂量依赖性减少。动物经辣椒素全身预处理后,辣椒素诱导的血管舒张被消除,而血管收缩增强。电子显微镜显示,急性暴露于辣椒素(10 μM)后硬脑膜中有退化的无髓轴突,这为辣椒素敏感的硬脑膜传入神经的存在及其可能的功能作用提供了支持。结果表明,辣椒素诱导的大鼠硬脑膜血管舒张是由感觉神经释放CGRP介导的,而血管收缩反应可能归因于辣椒素对血管平滑肌的直接作用。本研究首次证明辣椒素敏感的伤害性传入神经对硬脑膜血管舒张反应有显著贡献,并提示其在脑膜伤害感受中起重要作用。