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Hydrogen Sulfide Mediates Carotid body Response to Hypoxia
Author(s) -
Peng YingJie,
Nanduri Jayasri,
Raghuraman Gayatri,
Gadalla Moataz,
Kumar Ganesh,
Snyder Solomon,
Prabhakar Nanduri
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.669.21
Gaseous messengers, nitric oxide and carbon monoxide are implicated in O 2 sensing by the carotid body. In the present study, we examined the role of hydrogen sulfide (H 2 S) another gaseous messenger in the carotid body sensory response to hypoxia. Glomus cells from rat and mice carotid bodies expressed cystathionine γ‐lyase (CSE), an H 2 S generating enzyme. Hypoxia increased H 2 S generation in a stimulus‐dependent manner. Mice with genetic deletion of CSE displayed severely impaired carotid body and ventilatory responses to hypoxia as well as loss of hypoxia‐evoked H 2 S generation from the carotid body. Pharmacologic inhibition of CSE elicited a similar phenotype in mice and rats. Inhibition of hemeoxygenase‐2 in normoxia increased H 2 S generation, whereas a carbon monoxide donor inhibited hypoxia‐evoked H 2 S generation in the carotid body. These results demonstrate that a) hypoxia increases H2S generation via CSE, which mediates carotid body sensory response to hypoxia; and b) hypoxia‐evoked H 2 S generation require interaction of hemeoxygenase‐2 with CSE. Supported by HL‐90554, HL‐76537, HL‐86493 and HL‐089616.