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.