H 2 S mediates O 2 sensing in the carotid body
Open accessAbstract
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 (H 2 S) 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 γ-lyase (CSE), an H 2 S-generating enzyme, with hypoxia increasing H 2 S 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 H 2 S generation. Pharmacologic inhibition of CSE elicits a similar phenotype in mice and rats. Hypoxia-evoked H 2 S 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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Increasing evidence suggests that hydrogen sulfide can act as an oxygen sensor.
“Increasing evidence suggests that this evolutionary ancient gas can act as an oxygen sensor (423, 436).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [436]
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Placental Origins of Chronic Disease
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- Authors
- Peng, Y.-J., Nanduri, J., Raghuraman, G., Souvannakitti, D., Gadalla, M. M., Kumar, G. K., Snyder, S. H., & Prabhakar, N. R.
- Affiliations
- Center for Systems Biology for O2 sensing, Department of Medicine, University of Chicago, IL 60637; and
- University of Chicago (US)
- Department of Pharmacology and Molecular Sciences,
- Johns Hopkins University (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2010-05-24
- Volume
- 107
- Issue
- 23
- Pages
- 10719-10724
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2890835
- OpenAlex
- W2075366948
- Cited by
- 361
- References
- 34
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 7 · 2023: 18 · 2022: 12 · 2021: 22 · 2020: 13 · 2019: 19 · 2018: 27 · 2017: 17 · 2016: 28 · 2015: 42 · 2014: 32 · 2013: 34 · 2012: 44
- FWCI
- 15.60
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1z01da000226-02)
- National Heart, Lung, and Blood Institute (R01HL086493, P01HL090554, T32HL007653, HL-7653, HL90554, HL86493, R01HL076537)
- National Institute on Drug Abuse (DA 00074, DA 000226, K05DA000074)
- National Institute of General Medical Sciences (T32GM007309)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
- Health Sciences › Medicine › Physiology › Obstructive Sleep Apnea Research
- Keywords
- hydrogen sulfide, carotid body, oxygen sensing, hypoxia, cystathionine gamma-lyase, gasotransmitters, carbon monoxide, glomus cells, ventilatory response, adrenal medulla, catecholamine release
- MeSH terms
- Animals, Hypoxia, Carotid Body, Cystathionine gamma-Lyase, Hydrogen Sulfide, Male, Oxygen, Mice, Knockout, Mice, Rats
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