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Carbon monoxide (CO) and hydrogen sulfide (H2S) in hypoxic sensing by the carotid body

Authors
Journal
Respiratory Physiology & Neurobiology
1569-9048
Publisher
Elsevier
Publication Date
Volume
184
Issue
2
Identifiers
DOI: 10.1016/j.resp.2012.05.022
Keywords
  • Oxygen Sensing
  • Gas Messengers
  • K+ Channels
  • Calcium Signaling
Disciplines
  • Biology

Abstract

Abstract Carotid bodies are sensory organs for monitoring arterial blood oxygen (O2) 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 (H2S) in hypoxic sensing by the carotid body. Glomus cells, the primary site of O2 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 O2. 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 H2S generating enzyme. Exogenous application of H2S donors, like hypoxia, stimulate the carotid body activity and CSE knockout mice exhibit severely impaired sensory excitation by hypoxia, suggesting that CSE catalyzed H2S is an excitatory gas messenger. Hypoxia increases H2S generation in the carotid body, and this response was attenuated or absent in CSE knockout mice. HO inhibitor increased and CO donor inhibited H2S generation. It is proposed that carotid body response to hypoxia requires interactions between HO-2–CO and CSE–H2S systems.

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