K(+) channels in O(2) sensing and postnatal development of carotid body glomus cell response to hypoxia.

The sensitivity of carotid body chemoreceptors to hypoxia is low just after birth and increases over the first few weeks of the postnatal period. At present, it is believed that the hypoxia-induced excitation of carotid body glomus cells begins with the inhibition of the outward K(+) current via one or more O(2) sensors. Although the nature of the O(2) sensors and their signals that inhibit the K(+) current are not well defined, studies suggest that the postnatal maturation of the glomus cell response to hypoxia is largely due to the increased sensitivity of K(+) channels to hypoxia. As K(V), BK and TASK channels that are O(2)-sensitive contribute to the K(+) current, it is important to identify the O(2) sensor and the signaling molecule for each of these K(+) channels. Various O(2) sensors (mitochondrial hemeprotein, hemeoxygenase-2, NADPH oxidase) and associated signals have been proposed to mediate the inhibition of K(+) channels by hypoxia. Studies suggest that a mitochondrial hemeprotein is likely to serve as an O(2) sensor for K(+) channels, particularly for TASK, and that multiple signals may be involved. Thus, changes in the sensitivity of the mitochondrial O(2) sensor to hypoxia, the sensitivity of K(+) channels to signals generated by mitochondria, and/or the expression levels of K(+) channels are likely to account for the postnatal maturation of O(2) sensing by glomus cells.