Systemic hypoxia is a potentially lethal situation for the animal. To protect major organs from irreversible damage, the carotid body, a primary sensory organ for arterial hypoxia, sends a message to the central nervous system and induces various responses in cardiovascular, respiratory, renal, and endocrine systems (1). This is a unique feature of the carotid body: i.e., the consequences of oxygen sensing are not confined within the organ, but are used to serve other organs. Decades of investigations have tried to clarify characteristics of this unique organ, such as oxygen-sensing mechanisms, transduction pathways, and transmission of the information between the glomus cells of the carotid body and the sensory afferent neurons. At present, most investigators propose a model in which glomus cells, the chemosensory cells, release neurotransmitters as a result of an increase in intracellular Ca2+, ([Ca2+]i) in response to stimuli such as hypoxia. The resulting interaction of neurotransmitters and their receptors generates action potentials in the chemosensory afferent fiber. In this schema, neurotransmitters, their receptors, and ion channels are critical components. To date, much information has been gathered regarding the effects of hypoxia on several types of ion channels in glomus cells. However, it is still difficult to obtain a unified view of the mechanisms of chemoreception and chemotransduction in the carotid body. Perhaps a deeper understanding of the mechanisms involved in the hypoxic excitation of the carotid body can be gained by considering the fact that all channels and receptors are operating together, and their cross-talk, not the action of single component, determines the excitability of glomus cells. In this chapter we present an example of such interactions. In brief, we have found that cholinergic receptors modify the activity of voltage-gated K+ channels (Kv channels).
|Original language||English (US)|
|Title of host publication||Oxygen Sensing|
|Subtitle of host publication||Responses and Adaption to Hypoxia|
|Number of pages||19|
|State||Published - Jan 1 2003|
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