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Cardiovascular Research Advance Access originally published online on December 4, 2007
Cardiovascular Research 2008 77(4):774-781; doi:10.1093/cvr/cvm081
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

Ligand-dependent activation of ERβ lowers blood pressure and attenuates cardiac hypertrophy in ovariectomized spontaneously hypertensive rats

Virginija Jazbutyte1, Paula Anahi Arias-Loza1, Kai Hu1, Julian Widder1, Vijayakumar Govindaraj1, Christine von Poser-Klein1, Johann Bauersachs1, Karl-Heinrich Fritzemeier2, Christa Hegele-Hartung2, Ludwig Neyses3, Georg Ertl1 and Theo Pelzer1,*

1 Department of Medicine, University of Würzburg, Josef-Schneider Str. 2, D-97080 Würzburg, Germany
2 Schering AG, Berlin, Germany
3 Division of Cardiology, University of Manchester, Manchester, UK

* Corresponding author. Tel: +49 931 201 36112; fax: +49 931 201 36212. E-mail address: pelzer_t{at}klinik.uni-wuerzburg.de

Aims: The biological effects of oestrogens are mediated by two different oestrogen receptor (ER) subtypes, ER{alpha} and ERβ, which might play different, redundant, or opposing roles in cardiovascular disease. Previously, we have shown that the selective ER{alpha} agonist 16{alpha}-LE2 improves vascular relaxation, attenuates cardiac hypertrophy, and increases cardiac output without lowering elevated blood pressure in spontaneously hypertensive rats (SHR). Because ERβ-deficient mice exhibit elevated blood pressure and since the ERβ agonist 8β-VE2 attenuated hypertension in aldosterone-salt-treated rats, we have now tested the hypothesis that the isotype-selective ERβ agonist 8β-VE2 might be capable of lowering elevated blood pressure in ovariectomized SHR.

Methods and results: Treatment of ovariectomized SHR with 8β-VE2 for 12 weeks conferred no uterotrophic effects but lowered elevated systolic blood pressure (–38 ± 5 mmHg, n = 31, P < 0.001 vs. placebo) as well as peripheral vascular resistance (–31.3 ± 4.6%, P < 0.001 vs. placebo). 8β-VE2 enhanced aortic ERβ expression (+75.7 ± 7.1%, P < 0.01 vs. placebo), improved NO-dependent vasorelaxation, augmented phosphorylation of the vasodilator-stimulated phosphoprotein in isolated aortic rings (P < 0.05 vs. placebo), increased cardiac output (+20.4 ± 2.5%, P < 0.01 vs. placebo), and attenuated cardiac hypertrophy (–22.2 ± 3.2%, p < 0.01 vs. placebo). 8β-VE2, in contrast to oestradiol, did not enhance cardiac {alpha}-myosin heavy chain expression.

Conclusion: Ligand-dependent activation of ERβ confers blood pressure lowering effects in SHR that are superior to those of 17β-estradiol or the ER{alpha} agonist 16{alpha}-LE2 and attenuates cardiac hypertrophy primarily by a reduction of cardiac afterload without promoting uterine growth.

KEYWORDS Oestrogen receptor; Myocardium; Hypertrophy; Hypertension

Time for primary review: 26 days


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