TY - JOUR T1 - Carbon monoxide (CO) and hydrogen sulfide (H(2)S) in hypoxic sensing by the carotid body. A1 - Prabhakar,Nanduri R, Y1 - 2012/06/02/ PY - 2012/04/30/received PY - 2012/05/24/revised PY - 2012/05/27/accepted PY - 2012/6/6/entrez PY - 2012/6/6/pubmed PY - 2013/4/16/medline SP - 165 EP - 9 JF - Respiratory physiology & neurobiology JO - Respir Physiol Neurobiol VL - 184 IS - 2 N2 - 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. SN - 1878-1519 UR - https://www.unboundmedicine.com/medline/citation/22664830/Carbon_monoxide__CO__and_hydrogen_sulfide__H_2_S__in_hypoxic_sensing_by_the_carotid_body_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1569-9048(12)00136-X DB - PRIME DP - Unbound Medicine ER -