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- W2184088679 endingPage "L582" @default.
- W2184088679 startingPage "L575" @default.
- W2184088679 abstract "Nitric oxide (NO) is a potent vasodilator and inhibitor of vascular remodeling. Reduced NO production has been implicated in the pathophysiology of pulmonary hypertension, with endothelial NO synthase (NOS) knockout mice showing an increased risk for pulmonary hypertension. Because molecular oxygen (O2) is an essential substrate for NO synthesis by the NOSs and biochemical studies using purified NOS isoforms have estimated the Michaelis-Menten constant values for O2 to be in the physiological range, it has been suggested that O2 substrate limitation may limit NO production in various pathophysiological conditions including hypoxia. This review summarizes numerous studies of the effects of acute and chronic hypoxia on NO production in the lungs of humans and animals as well as in cultured vascular cells. In addition, the effects of hypoxia on NOS expression and posttranslational regulation of NOS activity by other proteins are also discussed. Most studies found that hypoxia limits NO synthesis even when NOS expression is increased." @default.
- W2184088679 created "2016-06-24" @default.
- W2184088679 creator A5011168502 @default.
- W2184088679 creator A5055741938 @default.
- W2184088679 date "2001-04-01" @default.
- W2184088679 modified "2023-10-15" @default.
- W2184088679 title "Nitric oxide production in the hypoxic lung" @default.
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- W2184088679 doi "https://doi.org/10.1152/ajplung.2001.280.4.l575" @default.
- W2184088679 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11237994" @default.
- W2184088679 hasPublicationYear "2001" @default.
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