Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 107, Issue 23, Pages 10719-10724Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1005866107
Keywords
cystathionine gamma-lyase; hydrogen sulfide; hypoxia; hemeoxygenase-2
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Funding
- National Institutes of Health [HL-76537, HL-90554, HL-86493, T32 GM007309]
- US Public Health Service [DA 000226, DA 00074]
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Gaseous messengers, nitric oxide and carbon monoxide, have been implicated in O-2 sensing by the carotid body, a sensory organ that monitors arterial blood O-2 levels and stimulates breathing in response to hypoxia. We now show that hydrogen sulfide (H2S) is a physiologic gasotransmitter of the carotid body, enhancing its sensory response to hypoxia. Glomus cells, the site of O-2 sensing in the carotid body, express cystathionine.-lyase (CSE), an H2S-generating enzyme, with hypoxia increasing H2S generation in a stimulus-dependent manner. Mice with genetic deletion of CSE display severely impaired carotid body response and ventilatory stimulation to hypoxia, as well as a loss of hypoxia-evoked H2S generation. Pharmacologic inhibition of CSE elicits a similar phenotype in mice and rats. Hypoxia-evoked H2S generation in the carotid body seems to require interaction of CSE with hemeoxygenase-2, which generates carbon monoxide. CSE is also expressed in neonatal adrenal medullary chromaffin cells of rats and mice whose hypoxia-evoked catecholamine secretion is greatly attenuated by CSE inhibitors and in CSE knockout mice.
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