Journal article
IL-6 Deficiency Protects Against Angiotensin II–Induced Endothelial Dysfunction and Hypertrophy
Arteriosclerosis, thrombosis, and vascular biology, Vol.27(12), pp.2576-2581
12/2007
DOI: 10.1161/ATVBAHA.107.153080
PMID: 17962626
Abstract
OBJECTIVE—The goal of this study was to test the hypothesis that IL-6 mediates the increases in superoxide, vascular hypertrophy, and endothelial dysfunction in response to angiotensin II (Ang II).
METHODS AND RESULTS—Responses of carotid arteries from control and IL-6–deficient mice were examined after acute (22-hour) incubation with Ang II (10 nmol/L) or chronic infusion of Ang II (1.4 mg/kg/d for 14 days). The hypertrophic response and endothelial dysfunction produced by Ang II infusion was markedly less in carotid arteries from IL-6–deficient mice than that in control mice. IL-6 deficiency also protected against endothelial dysfunction in response to acute (local) Ang II treatment (eg, 100 μmol/L acetylcholine produced 100±4 and 98±4% relaxation in vehicle-treated and 51±4 and 99±4% relaxation in Ang II–treated, control, and IL-6–deficient vessels, respectively). Endothelial dysfunction could be reproduced in vessels from IL-6–deficient mice with combined Ang II plus IL-6 (0.1 nmol/L) treatment. Increases in vascular superoxide and IL-6, as well as reductions in endothelial nitric oxide synthase mRNA expression, produced by Ang II were absent in IL-6–deficient mice.
CONCLUSIONS—These data demonstrate that IL-6 is essential for Ang II–induced increases in superoxide, endothelial dysfunction, and vascular hypertrophy.
Details
- Title: Subtitle
- IL-6 Deficiency Protects Against Angiotensin II–Induced Endothelial Dysfunction and Hypertrophy
- Creators
- Laura Schrader - From the Departments of Internal Medicine and Pharmacology, Cardiovascular Center, The University of Iowa Carver College of Medicine, Iowa CityDale KinzenbawAndrew JohnsonFrank FaraciSean Didion
- Resource Type
- Journal article
- Publication Details
- Arteriosclerosis, thrombosis, and vascular biology, Vol.27(12), pp.2576-2581
- Publisher
- American Heart Association, Inc
- DOI
- 10.1161/ATVBAHA.107.153080
- PMID
- 17962626
- ISSN
- 1079-5642
- eISSN
- 1524-4636
- Language
- English
- Date published
- 12/2007
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040214802771
Metrics
15 Record Views