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Acute oxygen sensing: diverse but convergent mechanisms in airway and arterial chemoreceptors

DOI: 10.1186/rr51

Keywords: carotid body, chemoreceptor, hypoxia, neuroepithelial body, O2 sensing

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Abstract:

Aerobic metabolism requires an adequate supply of O2, and rapid adaptation to changes in the partial pressures of inspired atmospheric gases is crucial to survival. During episodes of compromised O2 availability, numerous chemosensory systems, acting in concert, rapidly modulate pulmonary ventilation and perfusion to optimize the supply of O2 from alveolus to metabolising tissues. This review focuses on two key systems involved in this homeostatic response: the carotid bodies (CBs) and neuroepithelial bodies (NEBs), representative chemoreceptors of the arterial circulation and the airway, respectively [1,2]. So far, CBs and NEBs, together with pulmonary smooth muscle (which will not be examined in great depth here), have been the most extensively studied of O2-sensitive tissues, and recent investigations have provided major new insights into the expression and interactions of molecular components that link a decreased partial pressure of oxygen (pO2) to appropriate cellular responses in the circulation and respiratory systems.CBs are highly vascularised organs, located at the bifurcations of the common carotid arteries, that rapidly initiate increased activity in afferent chemosensory fibres of the carotid sinus nerve in response to systemic hypoxaemia. There is widespread agreement that the sensory elements of the CB are the type I (glomus) cells, which contain numerous transmitters and lie in synaptic contact with afferent sensory neurones [1,3]. Type I cells release catecholamines, acetylcholine and ATP in response to hypoxia to initiate afferent discharge [4]. Commonly located at airway bifurcations are NEBs, tight clusters of neurone-derived, transmitter-containing cells that synapse with branches of both afferent and efferent neurones. They evoke appropriate responses to airway hypoxia (as opposed to hypoxaemia) by initiating afferent information to the respiratory centres [5] and releasing peptides and amine modulators [particularly 5-hydroxytryptamine (serot

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