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- W1433346886 abstract "The goal of the present study was to test the hypothesis that heterozygous endothelial nitric oxide synthase (eNOS)-deficiency is associated with oxidative stress and endothelial dysfunction produced by interleukin-6 (IL-6). Carotid arteries from eNOS+/+ and eNOS+/- mice were incubated with either vehicle or interleukin-6 (100 or 300 nM) for 22 hrs. IL-6 produced concentration-dependent impairment (P<0.05) of responses to acetylcholine in eNOS+/- mice. For example, acetylcholine (100 µM) produced 89±1, 60±8, and 35±4% relaxation in arteries from eNOS+/- mice treated with vehicle, 100 nM IL-6, or 300 nM IL-6, respectively. Basal and NADPH-stimulated superoxide levels were also selectively increased in vessels from eNOS+/- mice incubated with IL-6. IL-6 had no effect (P>0.05) on endothelial responses or superoxide levels in eNOS+/+ mice. The effects of IL-6 were selective for endothelium as responses to nitroprusside were unaltered (P>0.05) by IL-6 or genotype. Taken together, these findings demonstrate that loss of a single eNOS gene predisposes blood vessels to the negative effects of IL-6. These findings are an example of eNOS haploinsufficiency and have important implications in disease states associated with reductions in eNOS expression and/or activity in combination with increases in IL-6, such as aging and obesity. Supported by NIH HL-089884 and HL-107632." @default.
- W1433346886 created "2016-06-24" @default.
- W1433346886 creator A5013221335 @default.
- W1433346886 date "2015-04-01" @default.
- W1433346886 modified "2023-09-28" @default.
- W1433346886 title "Interleukin‐6 Produces Oxidative Stress and Endothelial Dysfunction in the Absence of a Single Endothelial Nitric Oxide Synthase Gene" @default.
- W1433346886 doi "https://doi.org/10.1096/fasebj.29.1_supplement.971.10" @default.
- W1433346886 hasPublicationYear "2015" @default.
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