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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Chemoreceptor discharges and cytochrome redox changes of the rat carotid body: Role of heme ligands
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Chemoreceptor discharges and cytochrome redox changes of the rat carotid body: Role of heme ligands

机译：大鼠颈动脉化学感受器放电和细胞色素氧化还原变化：血红素配体的作用

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摘要

In superfused in vitro rat carotid body, we recorded chemoreceptor discharges and the redox state of cytochromes simultaneously to identify the primary oxygen- sensing protein controlling transmitter release and electrical activity of the carotid sinus nerve. These parameters were tested under the influence of heme ligands such as oxygen, cyanide, 4-(2-aminoethyl)-benzenesulfonyl fluoxide, and CO. During stimulation, there was an initial increase in discharge frequency followed by a decline or suppression of activity. Photometric changes lagged and were maintained as nerve activity decreased. Reducing mitochondrial cytochromes by cyanide or prolonged severe hypoxia, suppressed the chemo- receptor discharge. 4-(2-Aminoethyl)-benzenesulfonyl fluo- ride, a specific inhibitor of the phagocytic cytochrome b-558, also silenced the chemoreceptors after an initial excitation. CO increased the chemoreceptor discharge under normoxia, an effect inhibited by light, when the cytochromes were not reduced. When the discharges were depressed by severe hyp- oxia, exposure to light excited the chemoreceptors and the cytochromes were reduced. The rapidity of the chemosensory responses to light and lack of effect on dopamine release from type I cells led us to hypothesize that carotid body type I cells and the apposed nerve endings use different mechanisms for oxygen sensing: the nerve endings generate action potentials in association with membrane heme proteins whereas cyto- solic heme proteins signal the redox state, releasing modula- tors or transmitters from type I cells.
机译：在体外大鼠颈动脉融合体中，我们同时记录了化学感受器放电和细胞色素的氧化还原状态，以识别控制着颈动脉窦神经递质释放和电活动的主要氧敏感蛋白。这些参数是在血红素配体（如氧，氰化物，4-（2-氨基乙基）-苯磺酰氟和CO）的影响下进行测试的。在刺激过程中，放电频率最初有所增加，随后降低或抑制了活性。光度变化滞后，并随着神经活动的减少而得以维持。通过氰化物减少线粒体细胞色素或长时间严重缺氧可抑制化学受体的释放。吞噬细胞色素b-558的特异抑制剂4-（2-氨基乙基）-苯磺酰基氟在初始激发后也沉默了化学感受器。当细胞色素不减少时，CO增加了常氧下的化学感受器放电，这是受光抑制的效果。当严重缺氧抑制了放电时，暴露于光下会激发化学感受器和细胞色素的减少。对光的化学感应反应的快速性和对I型细胞释放多巴胺的影响不足，使我们假设颈动脉I型细胞和并置的神经末梢使用不同的机制来进行氧传感：神经末梢产生的动作电位与膜血红素蛋白，而细胞性血红素蛋白则指示氧化还原状态，从而释放I型细胞的调节剂或递质。

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