title: Role of nitric oxide in the control of mitochondrial function.
abstract: In summary, NO is capable of decreasing mitochondrial respiration in a variety of mammalian tissues. This effect is mediated primarily via binding of NO to the O2 binding site of cytochrome oxidase. This highly sensitive interaction presumably reflects a remnant homology between cytochrome oxidase and bacterial nitrate reductase. This effect has been demonstrated at physiologic levels of NO, highlighting the role for NO in the tonic control of cellular respiration. As this inhibition is dependent upon the levels figure: see text[ of NO and O2 in the tissue, various states of NO production and oxygen supply dictate the ultimate respiratory rate of the mitochondria. Furthermore, deviation from a physiologic NO: O2 may lead to an exacerbation of pathologic states, such as congestive heart failure and septic shock. Thus, NO may play a crucial role in the control of cellular respiration, providing an additional mechanism of action for this biologically diverse molecule that is distinct yet inseparable from its dilator effect on blood vessels.
authors.affiliation: Department of Physiology, New York Medical College, Valhalla 10595, USA.
authors.forename: P R
authors.initials: PR
authors.lastname: Forfia
authors.forename: T H
authors.initials: TH
authors.lastname: Hintze
authors.forename: M S
authors.initials: MS
authors.lastname: Wolin
authors.forename: G
authors.initials: G
authors.lastname: Kaley
mesh_terms: D000818:Animals; D003576:Electron Transport Complex IV / Q000378:metabolism; D006801:Humans; D008928:Mitochondria / Q000378:metabolism / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism / Q000502:physiology*; D010101:Oxygen Consumption
chemical_list: D009569:Nitric Oxide; D003576:Electron Transport Complex IV