Green P G, Luo J, Heller P, Levine J D
Department of Anatomy, University of California, San Francisco 94143.
Neuroscience. 1993 Jan;52(2):451-8. doi: 10.1016/0306-4522(93)90171-b.
We describe the contribution of various sympathetic post-ganglionic neuron mediators to bradykinin-induced plasma extravasation in the knee joint of the rat. Co-perfusion of the sympathetic post-ganglionic neuron mediators, norepinephrine or neuropeptide Y with bradykinin resulted in diminished plasma extravasation. In contrast, the putative sympathetic post-ganglionic neuron mediators of bradykinin-induced plasma extravasation, namely prostaglandin E2, ATP, the selective adenosine A2-receptor agonist, CGS21680 or the endothelium-derived relaxing factor (as its precursor L-arginine) all greatly enhanced bradykinin-induced plasma extravasation, but produced little or no increase in plasma extravasation administered alone. The data show that sympathetic post-ganglionic neuron-derived mediators may either inhibit or enhance plasma extravasation induced by bradykinin, and we hypothesize that differential release of mediators from the sympathetic post-ganglionic neuron terminal, in response to varying stimuli, regulates local plasma extravasation during inflammation.
我们描述了各种交感神经节后神经元介质对缓激肽诱导的大鼠膝关节血浆外渗的作用。交感神经节后神经元介质去甲肾上腺素或神经肽Y与缓激肽共同灌注导致血浆外渗减少。相比之下，缓激肽诱导血浆外渗的假定交感神经节后神经元介质，即前列腺素E2、ATP、选择性腺苷A2受体激动剂CGS21680或内皮衍生舒张因子（作为其前体L-精氨酸）均极大地增强了缓激肽诱导的血浆外渗，但单独给药时血浆外渗几乎没有增加或没有增加。数据表明，交感神经节后神经元衍生的介质可能抑制或增强缓激肽诱导的血浆外渗，并且我们推测，交感神经节后神经元末梢介质的差异释放，响应不同刺激，在炎症期间调节局部血浆外渗。
