López-Barneo José
Laboratorio de Investigaciones Biomédicas, Departamento de Fisiología and Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Avenida Manuel Siurot s/n E-41013 Seville, Spain.
Curr Opin Neurobiol. 2003 Aug;13(4):493-9. doi: 10.1016/s0959-4388(03)00093-x.
Carotid body glomus cells sense hypoxia through the inhibition of plasmalemmal K(+) channels, which leads to Ca(2+) influx and transmitter release. Although the mechanism of O(2) sensing remains enigmatic, it does not seem to depend on cellular redox status or inhibition of mitochondrial electron transport. Hypoxia inducible factors appear to be necessary for the expression of the O(2) sensor and carotid body remodeling in chronic hypoxia, but are not directly involved in acute O(2) sensing. Glomus cells are also rapidly activated by reductions of glucose concentration due to inhibition of K(+) channels. These cells function as combined O(2) and glucose sensors that help to prevent neuronal damage by acute hypoxia and/or hypoglycemia.
颈动脉体球细胞通过抑制质膜钾离子通道来感知缺氧，这会导致钙离子内流和神经递质释放。尽管氧气感知机制仍然神秘，但它似乎并不依赖于细胞氧化还原状态或线粒体电子传递的抑制。缺氧诱导因子似乎是慢性缺氧时氧气传感器表达和颈动脉体重塑所必需的，但并不直接参与急性氧气感知。由于钾离子通道受到抑制，球细胞也会因葡萄糖浓度降低而迅速被激活。这些细胞作为氧气和葡萄糖的联合传感器，有助于预防急性缺氧和/或低血糖引起的神经元损伤。
