Academic Journal
Endothelial Nox4 NADPH Oxidase Enhances Vasodilatation and Reduces Blood Pressure In Vivo
العنوان: | Endothelial Nox4 NADPH Oxidase Enhances Vasodilatation and Reduces Blood Pressure In Vivo |
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المؤلفون: | Ray, Robin, Murdoch, Colin E., Wang, Minshu, Santos, Celio X., Zhang, Min, Alom-Ruiz, Sara, Anilkumar, Narayana, Ouattara, Alexandre, Cave, Alison C., Walker, Simon J., Grieve, David J., Charles, Rebecca L., Eaton, Philip, Brewer, Alison C., Shah, Ajay M. |
المصدر: | Arteriosclerosis, Thrombosis, and Vascular Biology ; volume 31, issue 6, page 1368-1376 ; ISSN 1079-5642 1524-4636 |
بيانات النشر: | Ovid Technologies (Wolters Kluwer Health) |
سنة النشر: | 2011 |
الوصف: | Objective— Increased reactive oxygen species (ROS) production is involved in the pathophysiology of endothelial dysfunction. NADPH oxidase-4 (Nox4) is a ROS-generating enzyme expressed in the endothelium, levels of which increase in pathological settings. Recent studies indicate that it generates predominantly hydrogen peroxide (H 2 O 2 ), but its role in vivo remains unclear. Methods and Results— We generated transgenic mice with endothelium-targeted Nox4 overexpression (Tg) to study the in vivo role of Nox4. Tg demonstrated significantly greater acetylcholine- or histamine-induced vasodilatation than wild-type littermates. This resulted from increased H 2 O 2 production and H 2 O 2 -induced hyperpolarization but not altered nitric oxide bioactivity. Tg had lower systemic blood pressure than wild-type littermates, which was normalized by antioxidants. Conclusion— Endothelial Nox4 exerts potentially beneficial effects on vasodilator function and blood pressure that are attributable to H 2 O 2 production. These effects contrast markedly with those reported for Nox1 and Nox2, which involve superoxide-mediated inactivation of nitric oxide. Our results suggest that therapeutic strategies to modulate ROS production in vascular disease may need to separately target individual Nox isoforms. |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | English |
DOI: | 10.1161/atvbaha.110.219238 |
DOI: | 10.1161/ATVBAHA.110.219238 |
الاتاحة: | http://dx.doi.org/10.1161/atvbaha.110.219238 https://www.ahajournals.org/doi/full/10.1161/ATVBAHA.110.219238 |
رقم الانضمام: | edsbas.506C0467 |
قاعدة البيانات: | BASE |
DOI: | 10.1161/atvbaha.110.219238 |
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