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• W1998849608 abstract "Hypoxia inhibits β 2 -adrenergic receptor (β 2 -AR) signaling in a variety of tissues, but effects in alveolar epithelium are unclear. We therefore examined the effect of 24 h of hypoxia on β 2 -AR function in primary rat alveolar epithelial [alveolar type II (ATII)] cells. ATII cells were isolated, cultured to confluence, and incubated in normoxia or hypoxia (3% O 2 ) for 24 h. Hypoxia decreased maximal terbutaline-stimulated cAMP production by 37%; potency of terbutaline was not affected. Reoxygenation (3 h) reversed this effect. Density of β 2 -AR assessed by (−)-[ 125 I]iodocyanopindolol binding was decreased in hypoxia (−22%). Hypoxia did not affect terbutaline binding affinity to β 2 -AR. Hypoxia decreased G s protein levels by 27%, whereas no change was observed in G i1/2 , G i3 , and Gβ subunits. Forskolin-stimulated cAMP production was not inhibited by hypoxia. Pertussis toxin (PTX; 0.5 μg/ml, 2 h), an inhibitor of G i/o proteins, restored terbutaline-stimulated cAMP production of hypoxic ATII cells to normoxic control values. Cholera toxin (CTX)-stimulated G s protein activity did not change in hypoxia. Hypoxia increased the sensitivity of β 2 -AR to desensitization. These results indicate that despite the decrease in G s protein level G s protein was still functional and that hypoxia impairs β 2 -AR signaling due to an increased activity of G i/o proteins." @default.
• W1998849608 created "2016-06-24" @default.
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• W1998849608 date "2009-03-01" @default.
• W1998849608 modified "2023-10-15" @default.
• W1998849608 title "In vitro hypoxia impairs β₂-adrenergic receptor signaling in primary rat alveolar epithelial cells" @default.
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• W1998849608 doi "https://doi.org/10.1152/ajplung.90390.2008" @default.
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