Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 280, Issue 4, Pages L575-L582Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.2001.280.4.L575
Keywords
acute hypoxia; chronic hypoxia; pulmonary hypertension; nitric oxide synthase; isolated perfused lung
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Funding
- NHLBI NIH HHS [HL-14985] Funding Source: Medline
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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 (O-2) 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 O-2 to be in the physiological range, it has been suggested that O-2 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.
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