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• W2339630109 endingPage "L690" @default.
• W2339630109 startingPage "L683" @default.
• W2339630109 abstract "Hypoxic pulmonary vasoconstriction (HPV) matches lung perfusion with ventilation. Controversy exists whether decreased or increased reactive oxygen species may elicit HPV and from which source such oxygen metabolites are derived. In rabbit lungs, we detected transcripts of a nonphagocytic NADPH oxidase subunit homologous to mitogenic oxidase-1 (Mox1) or NADPH oxidase homolog 1 (NOH-1L). In perfused rabbit lungs, we employed 1) a new NADPH oxidase inhibitor [4-(2-aminoethyl)benzenesulfonyl fluoride (AEBSF; 100-600 microM)] and 2) the superoxide dismutase (SOD) inhibitors diethyldithiocarbamic acid (DETC; 100 microM to 10 mM) and triethylenetetramine (TETA; 1-25 mM). Specificity of these agents for HPV was investigated by comparison with U-46619-induced vasoconstrictions. AEBSF induced a transient increase in pulmonary arterial pressure with increased strength of HPV. Subsequent to this initial response, normoxic pulmonary arterial pressure was not affected and HPV was specifically suppressed. Whereas DETC turned out to act in a nonspecific fashion, TETA suppressed HPV specifically. These findings provide evidence of a role for a nonphagocytic NAD(P)H oxidase with superoxide and SOD-related hydrogen peroxide formation in HPV. Because HPV was inhibited but not mimicked by the inhibitors, increased rather than decreased superoxide and/or hydrogen peroxide formation is suggested as the hypoxia-provoked signaling event." @default.
• W2339630109 created "2016-06-24" @default.
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• W2339630109 date "2000-10-01" @default.
• W2339630109 modified "2023-10-17" @default.
• W2339630109 title "Hypoxic vasoconstriction in intact lungs: a role for NADPH oxidase-derived H₂O₂?" @default.
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• W2339630109 doi "https://doi.org/10.1152/ajplung.2000.279.4.l683" @default.
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