EDITORIAL

NO, hypoxia, and superoxide

Nitric oxide, hypoxia, and superoxide: the good, the bad, and the ugly!

R A Dweik

Correspondence to:
Correspondence to:
Dr R A Dweik
Department of Pulmonary, Allergy, and Critical Care Medicine, The Cleveland Clinic Foundation, 9500 Euclid Avenue/A90, Cleveland, Ohio 44195, USA; dweikr@ccf.org

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A possible role for NO in ARDS

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Abbreviations: ARDS, acute respiratory distress syndrome; FAD, flavin adenine dinucleotide; FMN, flavin mononucleotide; K_MO₂, Michaelis constant; NADPH, reduced nicotinamide-adenine dinucleotide phosphate; NO, nitric oxide; NOS, nitric oxide synthase; O₂^–, superoxide; ONOO^–, peroxynitrite; ROS, reactive oxygen species; SOD, superoxide dismutases

Keywords: nitric oxide; hypoxia; superoxide; pulmonary artery; acute respiratory distress syndrome (ARDS)

The first 150 words of the full text of this article appear below.

Nitric oxide (NO) is endogenously synthesised by nitric oxide synthases (NOS) which convert L-arginine to L-citrulline and NO. Three NOS isoforms (types I, II and III) have been identified and all of them are expressed in the human lung.^1–8 NOS I (nNOS) and III (eNOS) are constitutively expressed in tissues and are dependent on increases in intracellular calcium for enzyme activation while NOS II (iNOS) is an inducible form that is calcium independent (table 1).⁹ All NOS isoforms require oxygen, NADPH, FAD, FMN, tetrahydrobiopterin, and calmodulin for activity.^1,9 NO is recognised to have a key role in virtually all aspects of lung biology and has been implicated in the pathophysiology of lung diseases.^{1,4,6,10–15} It is involved in pulmonary neurotransmission, host defence and bacteriostasis, airway and vascular smooth muscle relaxation, pulmonary capillary leak, inflammation, mucociliary clearance, airway mucus secretion, and cytotoxicity.^4,6,14

View this table: [in this window] [in a new window]   Table 1  Nitric oxide synthase . . . [Full text of this article]

 

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