McDonald D M
Fed Proc. 1980 Jul;39(9):2627-35.
Several neural and vascular mechanisms regulate the sensitivity of carotid body chemoreceptors to hypoxia, hypercapnia, and acidosis. Factors that control blood flow and oxygen delivery in the carotid body along with those that augment or diminish catecholamine release from glomus cells can have major effects on chemoreceptor function. In addition, the sensory nerves themselves may participate in the regulation of chemoreceptor sensitivity. A portion of the carotid body's sensory nerves are presynaptic to glomus cells. In response to stimulation, the sensory nerve terminals exhibit ultrastructural changes that resemble changes associated with increased release of transmitter from motor nerves: 1) the number of small (synaptic) vesicles decreases; and 2) coated vesicles and coated regions of cisternal membrane increase in number during stimulation. If sensory nerves of the carotid body release a neurotransmitters, sensory nerve activity could influence glomus cell secretion of catecholamines or other substances tha modify chemoreceptor sensitivity. Such an effect could be produced in the carotid body by hypoxia and other conditions that stimulate the sensory nerves or it could result from antidromic activity evoked in the sensory nerves by primary afferent depolarization of their terminals in the CNS.
几种神经和血管机制调节颈动脉体化学感受器对缺氧、高碳酸血症和酸中毒的敏感性。控制颈动脉体血流和氧气输送的因素,以及那些增加或减少球细胞儿茶酚胺释放的因素,可对化学感受器功能产生重大影响。此外,感觉神经本身可能参与化学感受器敏感性的调节。颈动脉体的一部分感觉神经在球细胞之前形成突触。受到刺激时,感觉神经末梢会出现超微结构变化,这些变化类似于与运动神经递质释放增加相关的变化:1)小(突触)囊泡数量减少;2)在刺激过程中,包被囊泡和池膜的包被区域数量增加。如果颈动脉体的感觉神经释放一种神经递质,感觉神经活动可能会影响球细胞儿茶酚胺或其他改变化学感受器敏感性的物质的分泌。这种效应可能由缺氧和其他刺激感觉神经的情况在颈动脉体中产生,或者可能是由中枢神经系统中感觉神经末梢的初级传入去极化在感觉神经中诱发的逆向活动导致的。