Lahiri S, Roy A, Rozanov C, Mokashi A
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6085, USA.
Brain Res. 1998 May 25;794(1):162-5. doi: 10.1016/s0006-8993(98)00276-5.
According to the membrane channel hypothesis of carotid body O2 chemoreception, hypoxia suppresses K+ currents leading to cell depolarization, [Ca2+]i rise, neurosecretion, increased neural discharge from the carotid body. We show here that tetraethylammonium (TEA) plus 4-aminopyridine (4-AP) which suppressed the Ca2+ sensitive and other K+ currents in rat carotid body type I cells, with and without low [Ca2+]o plus high [Mg2+]o, did not essentially influence low PO2 effects on [Ca2+]i and chemosensory discharge. Thus, hypoxia may suppress the K+ currents in glomus cells but K+ current suppression of itself does not lead to chemosensory excitation. Therefore, the hypothesis that K+-O2 current is linked to events in chemoreception is not substantiated. K+-O2 current is an epiphemenon which is not directly linked with O2 chemoreception.
根据颈动脉体氧化学感受的膜通道假说，低氧抑制钾离子电流，导致细胞去极化、细胞内钙离子浓度升高、神经分泌以及颈动脉体神经放电增加。我们在此表明，四乙铵（TEA）加4-氨基吡啶（4-AP）可抑制大鼠颈动脉体I型细胞中对钙离子敏感的钾离子电流及其他钾离子电流，无论细胞外钙离子浓度降低及镁离子浓度升高与否，它们对低氧分压对细胞内钙离子浓度及化学感受性放电的影响并无实质作用。因此，低氧可能会抑制球细胞中的钾离子电流，但钾离子电流的抑制本身并不会导致化学感受性兴奋。所以，钾离子-氧电流与化学感受过程相关事件相联系的假说并未得到证实。钾离子-氧电流是一种附带现象，与氧化学感受并无直接关联。
Zotero 插件