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Cardiovascular Research Advance Access [Accepted Manuscript] published online on September 19, 2007
Cardiovascular Research, doi:10.1093/cvr/cvm021
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CHRONIC ANGIOTENSIN IV TREATMENT REVERSES ENDOTHELIAL DYSFUNCTION IN APOE-DEFICIENT MICE

Antony Vinh, Robert E. Widdop, Grant R. Drummond and Tracey A. Gaspari

Department of Pharmacology, Monash University, Victoria 3800, Australia

Correspondence: Assoc Prof Robert Widdop, Department of Pharmacology, Building 13E, Monash University, Clayton, Victoria 3800, Australia. Ph: +613 9905 4858, Fax: +613 9905 5851, Email: Robert.Widdop{at}med.monash.edu.au

Objectives: Endothelial dysfunction is considered a surrogate marker for cardiovascular disease. Angiotensin II, the principal hormone of the renin angiotensin system, is known to promote atherogenesis. However, other angiotensin peptide fragments such as angiotensin IV possess biological activity that may in fact counter-regulate the actions of angiotensin II. Therefore, we investigated the role of angiotensin IV on the development of endothelial dysfunction in apolipoprotein E-deficient (ApoE–/–) mice.

Methods and results: In contrast to their wild-type control, ApoE–/– mice were fed a high fat diet to exacerbate endothelial dysfunction, evidenced by impaired endothelium-dependent vasodilation. Chronic infusion of angiotensin IV (1.44 mg/kg/day) in ApoE–/– mice for 2 weeks resulted in significant improvements in endothelial function. Angiotensin IV treatment markedly decreased superoxide levels (dihydroethidium staining fluorescence and L-012 chemiluminescence) and increased endothelial nitric oxide synthase expression (immunoreactivity and Western blotting) in aortic tissue. Co-treatment of angiotensin IV with either the AT4 receptor antagonist divalinal-Ang IV or the AT2 receptor antagonist PD123319 attenuated these changes, indicating involvement of both the AT4 and AT2 receptors.

Conclusions: Chronic angiotensin IV treatment in ApoE–/– mice evoked a marked vasoprotective effect that appeared to be mediated by improved NO bioavailability due to AT4 and/or AT2 receptor stimulation.

Time for primary review: 18 days


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