Abstract
In adult humans, acute isocapnic hypoxia induces a brisk ventilatory response. This acute hypoxic response or AHR originates at the peripheral chemoreceptors of the carotid bodies.1,2 The full mechanisms of oxygen sensing at the carotid bodies (CB) is still poorly understood. At present it is thought that membrane ion channels (e.g. potassium channels) are critically involved and that low oxygen inhibits various K+-currents through the CB type I cell membrane (see reference #3 and references cited therein). This causes membrane depolarization and consequently the influx of calcium ions into the cell and the activation of a complex cascade of events within the type I cell. At the end of this cascade, the cell releases neurotransmitters (e.g., acetylcholine and ATP) which activate postsynaptic receptors located on afferent endings of the carotid sinus nerve.
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Dahan, A., Romberg, R., Sarton, E., Teppema, L. (2004). Antioxidants Prevent Blunting of Hypoxic Ventilatory Response by Low-Dose Halothane. In: Champagnat, J., Denavit-Saubié, M., Fortin, G., Foutz, A.S., Thoby-Brisson, M. (eds) Post-Genomic Perspectives in Modeling and Control of Breathing. Advances in Experimental Medicine and Biology, vol 551. Springer, Boston, MA. https://doi.org/10.1007/0-387-27023-X_33
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DOI: https://doi.org/10.1007/0-387-27023-X_33
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