Hydrogen sulfide and oxygen sensing in the cardiovascular system

Kenneth R. Olson, Nathan L. Whitfield

Research output: Contribution to journalReview articlepeer-review

110 Scopus citations

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 (H2S) as the O2-sensitive couple. Support for this hypothesis includes the similarity of effects of hypoxia and H2S on a variety of tissues, augmentation of hypoxic responses by precursors of H2S production and their inhibition by inhibitors of H2S synthesis, and the rapid consumption of H 2S by O2 in the range of intracellular/mitochondrial Po2. These studies also indicate that, under normoxic conditions, it is doubtful that free H2S has longer than a transient existence in tissue or extracellular fluid. Antioxid. Redox Signal. 12, 1219-1234.

Original languageEnglish (US)
Pages (from-to)1219-1234
Number of pages16
JournalAntioxidants and Redox Signaling
Volume12
Issue number10
DOIs
StatePublished - May 15 2010

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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