Abstract：
:Carotid bodies are sensory organs for monitoring arterial blood oxygen (O(2)) levels, and the ensuing reflexes maintain cardio-respiratory homeostasis during hypoxia. This article provides a brief update of the role of carbon monoxide (CO) and hydrogen sulfide (H(2)S) in hypoxic sensing by the carotid body. Glomus cells, the primary site of O(2) sensing in the carotid body express heme oxygenase-2 (HO-2), a CO catalyzing enzyme. HO-2 is a heme containing enzyme and has high affinity for O(2). Hypoxia inhibits HO-2 activity and reduces CO generation. Pharmacological and genetic approaches suggest that CO inhibits carotid body sensory activity. Stimulation of carotid body activity by hypoxia may reflect reduced formation of CO. Glomus cells also express cystathionine γ-lyase (CSE), an H(2)S generating enzyme. Exogenous application of H(2)S donors, like hypoxia, stimulate the carotid body activity and CSE knockout mice exhibit severely impaired sensory excitation by hypoxia, suggesting that CSE catalyzed H(2)S is an excitatory gas messenger. Hypoxia increases H(2)S generation in the carotid body, and this response was attenuated or absent in CSE knockout mice. HO inhibitor increased and CO donor inhibited H(2)S generation. It is proposed that carotid body response to hypoxia requires interactions between HO-2-CO and CSE-H(2)S systems.
journal_name
Respir Physiol Neurobioljournal_title
Respiratory physiology & neurobiologyauthors
Prabhakar NRdoi
10.1016/j.resp.2012.05.022subject
Has Abstractpub_date
2012-11-15 00:00:00pages
165-9issue
2eissn
1569-9048issn
1878-1519pii
S1569-9048(12)00136-Xjournal_volume
184pub_type
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