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Cardiovascular Research Advance Access [Accepted Manuscript] published online on December 4, 2007
Cardiovascular Research, doi:10.1093/cvr/cvm081
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Ligand-dependent activation of ERβ lowers blood pressure and attenuates cardiac hypertrophy in ovariectomized SHR

Virginija Jazbutyte, MSc1, Paula Anahi Arias-Loza, MSc1, Kai Hu, MD1, Julian Widder, MD1, Vijayakumar Govindaraj, MSc1, Christine von Poser-Klein, MD1, Johann Bauersachs, MD1, Karl-Heinrich Fritzemeier, PhD2, Christa Hegele-Hartung, MD-PhD2, Ludwig Neyses, MD3, Georg Ertl, MD1 and Theo Pelzer, MD1,

1 Department of Medicine, University of Würzburg, Germany
2 Schering AG Berlin / Germany
3 Division of Cardiology, University of Manchester UK

Corresponding author: Theo Pelzer MD Department of Medicine, University of Würzburg Josef-Schneider Str. 2, D-97080 Würzburg, Germany phone: +49-931-201-36112 fax: +49-931-201-36212 e-mail: pelzer_t{at}klinik.uni-wuerzburg.de

Aims: The biological effects of estrogens are mediated by two different estrogen 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 estradiol, did not enhance cardiac {alpha}-myosin heavy chain expression.

Conclusions: 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.

Time for primary review: 26


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