2007
DOI: 10.1161/atvbaha.107.153080
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IL-6 Deficiency Protects Against Angiotensin II–Induced Endothelial Dysfunction and Hypertrophy

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 i… Show more

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Cited by 167 publications
(214 citation statements)
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“…Angiotensin II (AngII) is the major effector peptide in the RAAS, which is well known as a potent vasoconstrictor. As previously described, chronic AngII treatment caused an elevation in the mean arterial pressure, prostaglandin induction which lead to endothelial dysfunction and oxidative stress (King & Fink 2006, Schrader et al 2007, Hernán-dez et al 2002, Touyz & Schiffrin 1999. We have previously shown that in addition to AngII mediated vasoconstriction, it also activates other pathways including enhancing carbon monoxide release (CO) by increasing HO-I (Heme oxygenase I), which leads to persistent hypertension (Quadri et al 2013).…”
Section: Introductionmentioning
confidence: 89%
“…Angiotensin II (AngII) is the major effector peptide in the RAAS, which is well known as a potent vasoconstrictor. As previously described, chronic AngII treatment caused an elevation in the mean arterial pressure, prostaglandin induction which lead to endothelial dysfunction and oxidative stress (King & Fink 2006, Schrader et al 2007, Hernán-dez et al 2002, Touyz & Schiffrin 1999. We have previously shown that in addition to AngII mediated vasoconstriction, it also activates other pathways including enhancing carbon monoxide release (CO) by increasing HO-I (Heme oxygenase I), which leads to persistent hypertension (Quadri et al 2013).…”
Section: Introductionmentioning
confidence: 89%
“…IL-6 is needed for polarization of T H 17 cells, and mice lacking this cytokine have lower BP and less endothelial dysfunction in response to Ang II infusion. 52,53 IL-6 may also increase BP by stimulating epithelial sodium channels in collecting duct cells. 54 Interestingly, in response to a combination of high-level Ang II infusion and DOCA salt administration, IL-17 deficiency can have adverse effects.…”
Section: T H 1 and T Hmentioning
confidence: 99%
“…To validate IS-induced endothelial dysfunction, thoracic aortic rings obtained from male Wistar rats aged 10 weeks were incubated in Dulbecco's modified eagle's medium (DMEM) with or without 250 mg ml À1 IS (SigmaAldrich, Tokyo, Japan), containing 120 U ml À1 penicillin, 120 mg ml À1 streptomycin, 50 mg ml À1 polymyxin B and 1% fetal bovine serum, for 5 h at 37 1C (n¼4), as described earlier. 24,25 The IS concentration and incubation time accepted in this study were the maximum of those described in earlier in vitro studies. 26,27 Vascular responses were then examined.…”
Section: Endothelium-dependent Vascular Responsesmentioning
confidence: 99%