López-Barneo J, Pardal R, Montoro R J, Smani T, García-Hirschfeld J, Ureña J
Departamento de Fisiología Médica y Biofisica, Universidad de Sevilla, Facultad de Medicina, Spain.
Respir Physiol. 1999 Apr 1;115(2):215-27. doi: 10.1016/s0034-5687(99)00016-x.
Ion channels are known to participate in the secretory or mechanical responses of chemoreceptor cells to changes in oxygen tension (P(O2)). We review here the modifications of K+ and Ca2+ channel activity and the resulting changes in cytosolic [Ca2+] induced by low P(O2) in glomus cells and arterial smooth muscle which are well known examples of O2-sensitive cells. Glomus cells of the carotid body behave as presynaptic-like elements where hypoxia produces a reduction of K+ conductance leading to enhanced membrane excitability, Ca2+ entry and release of dopamine and other neurotransmitters. In arterial myocytes, hypoxia can inhibit or potentiate Ca2+ channel activity, thus regulating cytosolic [Ca2+] and contraction. Ca2+ channel inhibition is observed in systemic myocytes and most conduit pulmonary myocytes, whereas potentiation is seen in a population of resistance pulmonary myocytes. The mechanism whereby O2 modulates ion channel activity could depend on either the direct allosteric modulation by O2-sensing molecules or redox modification by reactive chemical species.
已知离子通道参与化学感受器细胞对氧分压（P(O2)）变化的分泌或机械反应。在此，我们综述低P(O2)在球细胞和动脉平滑肌中引起的K+和Ca2+通道活性改变以及由此导致的胞质[Ca2+]变化，球细胞和动脉平滑肌是众所周知的对氧敏感的细胞例子。颈动脉体的球细胞表现为突触前样元件，其中缺氧会导致K+电导降低，从而增强膜兴奋性、Ca2+内流以及多巴胺和其他神经递质的释放。在动脉肌细胞中，缺氧可抑制或增强Ca2+通道活性，从而调节胞质[Ca2+]和收缩。在全身肌细胞和大多数肺传导肌细胞中观察到Ca2+通道抑制，而在一群肺阻力肌细胞中则观察到增强。氧气调节离子通道活性的机制可能取决于氧气传感分子的直接变构调节或活性化学物质的氧化还原修饰。
