Abstract
The carotid body (CB) is a chemosensory organ which detects a decrease in PaO2 or pHa and increases spiking levels on the carotid sinus nerve. Chemosensitivity normally increases after birth but this maturation is impaired by post-natal exposure to hyperoxia, resulting in a large reduction in spiking rates during normoxia and hypoxia (Donnelly, 2005) and reduction in carotid type I cell depolarization in response to anoxia (Kim, 2003). Previous studies have indicated that detection of hypoxia or acidity is mediated by modulation of a leak potassium conductance of which TASK-1 and TASK-3 are likely candidates. Accordingly, we hypothesized that post-natal hyperoxia exposure will alter the developmental profile of TASK channels within the carotid body cells.
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KIM, I., DONNELLY, D.F., CARROLL, J.L. (2006). Modulation of Gene Expression in Subfamilies of TASK K+ Channels by Chronic Hyperoxia Exposure in Rat Carotid Body. 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_6
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DOI: https://doi.org/10.1007/0-387-31311-7_6
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