Abstract
Ventilation is closely tied to PaCO2 and PaO2 via a feedback control mechanism. Most importantly, changes in PCO2 and/or H+ (pH) are sensed by the central nervous system (CNS) resulting in directly related changes in ventilation. The magnitude of this response relative to the stimulus is known as, “central ventilatory chemosensitivity.” Several electrophysiological studies have demonstrated that chemosensitive neurons – i.e. neurons that change their electrical activity in response to a shift of PCO2/pH – are widely distributed throughout the brainstem (Bernard and Nattie, 1996; Coates and Nattie, 1993; Dean et al., 1989, 1990; Kawai et al., 1996; Oyamada et al., 1998, 1999; Richerson, 1995), suggesting that they could be the central CO2/pH sensors that regulate ventilation. In addition, PaO2 levels are inversely related to ventilation. The type I cells of the carotid body serve as the main sensors stimulating ventilation when PaO2 declines (“peripheral ventilatory chemosensitivity”). The afferent inputs from these PCO2/pH- or PO2-sensitive cells converge at the respiratory center located in the brainstem, where the generation of respiratory neural activity is integrated.
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OYAMADA, Y., YAMAGUCHI, K., MURAI, M., ISHIZAKA, A., OKADA, Y. (2006). Potassium Channels in the Central Control of Breathing. In: Hayashida, Y., Gonzalez, C., Kondo, H. (eds) THE ARTERIAL CHEMORECEPTORS. ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY, vol 580. Springer, Boston, MA. https://doi.org/10.1007/0-387-31311-7_52
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DOI: https://doi.org/10.1007/0-387-31311-7_52
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