The role of nitric oxide in carotid chemoreception.
The role of nitric oxide in carotid chemoreception.
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一氧化氮在颈动脉化学感受中的作用。
DOI：
10.1159/000109430
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Fidone,SJ
中科院分区：
文献类型：
--
作者：
Wang,ZZ;Dinger,BG;Stensaas,LJ;Fidone,SJ
对猫和大鼠颈动脉体的免疫细胞化学和组织化学研究揭示了与化学感应 I 型细胞小叶以及颈动脉体脉管系统相关的一氧化氮合酶 (NOS) 阳性神经纤维丛。 NOS 阳性纤维起源于（1）位于颈动脉体中的自主神经元，沿着颈动脉窦神经（CNS）和第九脑神经分布，终止于颈动脉体血管的外膜层，以及（2）来自岩神经节（第九神经）的单极感觉神经元。颈动脉体与 NO 前体 3H-精氨酸一起孵育，产生 3H-瓜氨酸，这是 NO 合成的可检测副产物。此外，中枢神经系统的电刺激或颈动脉体暴露于低氧培养介质会增加 3 H-瓜氨酸的形成。毫摩尔浓度的 L-精氨酸可抑制缺氧引起的化学感受器活性，这种作用可被特异性 NOS 拮抗剂 L-NG-硝基精氨酸甲酯（L-NAME，0.1 mM）逆转。 CNS C 纤维的电刺激可提高颈动脉体脉管系统和 I 型细胞小叶中的环 GMP。在 L-NAME 存在的刺激过程中，环状 GMP 的产生减少，这一发现与已知的 NO 激活可溶形式鸟苷酸环化酶的能力一致。进一步的研究表明，短暂（< 1 分钟）刺激中枢神经系统 C 纤维会抑制灌注/灌流体外颈动脉体制剂中的基础化学感受器放电，而需要长时间（> 5 分钟）刺激才能抑制对缺氧的反应。 L-NAME 可逆转抑制作用。我们综合解剖学、神经药理学和电生理学数据表明，NO 在介导 CNS 抑制中发挥双重作用，一是通过其对器官脉管系统的作用，二是通过对化学感应 I 型细胞的直接影响。前一种途径涉及胆碱能/NOS 假定副交感自主神经元，而后者可能由轴突反射或化学感应神经末梢的初级传入去极化介导。
Immunocytochemical and histochemical studies of cat and rat carotid bodies have revealed a plexus of nitric oxide synthase (NOS)-positive nerve fibers associated with lobules of chemosensory type I cells as well as with the carotid body vasculature. NOS-postive fibers originate from (1) autonomic neurons located in the carotid body and distributed along the carotid sinus nerve (CNS) and IXth cranial nerve which terminate in the adventitial layer of carotid body blood vessels, and (2) from unipolar sensory neurons of the petrosal (IXth nerve) ganglion. Carotid bodies incubated with the NO precursor,3H-arginine, yield3H-citrulline, the detectable coproduct of NO synthesis. Furthermore, electrical stimulation of the CNS or exposure of carotid bodies to hypoxic incubation media elevates3H-citrulline formation. Millimolar concentrations ofL-arginine inhibit chemoreceptor activity evoked by hypoxia, an effect which is reversed by the specific NOS antagonist,L-NG-nitroarginine methylester (L-NAME, 0.1 mM). Electrical stimulation of CNS C fibers elevates cyclic GMP in the carotid body vasculature and lobules of type I cells. Cyclic GMP production is reduced during stimulation in the presence ofL-NAME, a finding consistent with the known ability of NO to activate a soluble form of guanylate cyclase. Further studies showed that brief (< 1 min) stimulation of CNS C fibers inhibits basal chemoreceptor discharge in a perfused/ superfused in vitro carotid body preparation, whereas prolonged (> 5 min) stimulation is required to inhibit the response to hypoxia. The inhibitory effect is reversed byL-NAME. Our combined anatomical, neuropharmacological and electrophysiological data suggest that NO plays a dual role in mediating CNS inhibition, one via its actions on the organ''s vasculature and the other through direct effects on the chemosensory type I cells. The former pathway involves cholinergic/NOS presumptive parasympathetic autonomic neurons, while the latter may be mediated by axon reflex or primary affarent depolarization of chemosensory nerve terminals.