1. Hydrogen sulfide and oxygen sensing in the cardiovascular system.
- Author
-
Olson KR and Whitfield NL
- Subjects
- Air Pollutants metabolism, Animals, Blood Vessels metabolism, Carotid Body cytology, Carotid Body metabolism, Cell Hypoxia physiology, Chemoreceptor Cells cytology, Chromaffin Cells metabolism, Humans, Ischemic Preconditioning, Myocardial, Oxidation-Reduction, Signal Transduction physiology, Cardiovascular System metabolism, Chemoreceptor Cells metabolism, Homeostasis physiology, Hydrogen Sulfide metabolism, Oxygen metabolism
- 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.
- Published
- 2010
- Full Text
- View/download PDF