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Hydrogen Sulfide and Oxygen Sensing in the Cardiovascular System
Abstract
Vertebrate cardiorespiratory homeostasis is inextricably dependent upon specialized cells that provide feedback on oxygen status in the tissues, blood, and on occasion, environment. These "oxygen sensing" cells include chemoreceptors and oxygen-sensitive chromaffin cells that initiate cardiorespiratory reflexes, vascular smooth muscle cells that adjust perfusion to metabolism or ventilation, and other cells that condition themselves in response to episodic hypoxia. Identification of how these cells sense oxygen and transduce this into the appropriate physiological response has enormous clinical applicability, but despite intense research there is no consensus regarding the initial hypoxia-effector coupling mechanism. This review examines an alternative mechanism of oxygen sensing using oxidation of endogenously produced hydrogen sulfide (H(2)S) as the O(2)-sensitive couple. Support for this hypothesis includes the similarity of effects of hypoxia and H(2)S on a variety of tissues, augmentation of hypoxic responses by precursors of H(2)S production and their inhibition by inhibitors of H(2)S synthesis, and the rapid consumption of H(2)S by O(2) in the range of intracellular/mitochondrial Po(2). These studies also indicate that, under normoxic conditions, it is doubtful that free H(2)S has longer than a transient existence in tissue or extracellular fluid.
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“Since H2S is oxidatively inactivated by the action of sulfide-quinoneoxidoreductase in mitochondria”
From On the chemical biology of the nitrite/sulfide interaction (2015) · cites this paper as [99]
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“while its formation is essentially oxygen independent [99,100]”
From On the chemical biology of the nitrite/sulfide interaction (2015) · cites this paper as [99]
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Hydrogen Sulfide as an O2 Sensor: A Critical Analysis
Prieto‐Lloret, J., & Aaronson, P. I. (2017) · Advances in experimental medicine and biology · doi:10.1007/978-3-319-63245-2_15 · Cited by 10
Metadata
- Authors
- Olson, K. R., & Whitfield, N. L.
- Affiliations
- Indiana University South Bend (US)
- University of Notre Dame (US)
- Corresponding author
- Olson, Kenneth R.
- ORCID
- Olson, Kenneth R.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2010-05
- Volume
- 12
- Issue
- 10
- Pages
- 1219-1234
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- OpenAlex
- W2076177365
- Cited by
- 136
- References
- 76
- Citations by year
- 2025: 3 · 2024: 1 · 2023: 6 · 2022: 4 · 2021: 5 · 2020: 4 · 2019: 3 · 2018: 2 · 2017: 6 · 2016: 6 · 2015: 10 · 2014: 15 · 2013: 20 · 2012: 17
- FWCI
- 8.90
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Antioxidants and Redox Signaling (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- hydrogen sulfide, oxygen sensing, hypoxia, chemoreceptors, vascular smooth muscle cells, hydrogen sulfide oxidation, mitochondrial oxygen consumption, redox signaling
- MeSH terms
- Air Pollutants, Animals, Blood Vessels, Cardiovascular System, Carotid Body, Chemoreceptor Cells, Homeostasis, Humans, Hydrogen Sulfide, Oxidation-Reduction, Oxygen, Signal Transduction, Cell Hypoxia, Ischemic Preconditioning, Myocardial, Chromaffin Cells
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