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European Journal of Heart Failure 2005 7(7):1079-1084; doi:10.1016/j.ejheart.2005.03.004
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© 2005 European Society of Cardiology

The influence of oestrogen-deficiency and ACE inhibition on the progression of myocardial hypertrophy in spontaneously hypertensive rats

van Eickels Martina, Schreckenberg Rolfb, Pieter A. Doevendansc, Rainer Meyerd, Christian Grohéa and Klaus-Dieter Schlüterb,*

a Medizinische Universitäts-Poliklinik, Universitätsklinikum Bonn Germany
b Physiologisches Institut, Justus-Liebig-Universität Giessen Aulweg 129, 35392 Giessen, Germany
c Department of Cardiology, Heart-Lung Centrum Utrecht, The Netherlands
d Physiologisches Institut II, Universitätsklinikum Bonn Germany

* Corresponding author. Tel.: +49 641 9947212; fax: +49 641 9947219. E-mail address: Klaus-Dieter.Schlueter{at}physiologie.med.uni-giessen.de


  Abstract

Background: ACE inhibitors are widely used to antagonize the biological activity of angiotensin II in hypertensive heart disease. Oestrogen reduces angiotensin type 1 receptor expression, and thereby modifies angiotensin signalling.

Aim: To investigate the interaction of oestrogen status and ACE inhibition on the development of left ventricular hypertrophy and expression of transforming growth factor (TGF)-β1 in female spontaneously hypertensive rats (SHR).

Methods and results: Intact female SHR, ovariectomised SHR, and ovariectomised SHR with 17β-oestradiol (E2) replacement therapy were either treated with placebo or the ACE inhibitor moexiprilat. Blood pressure, left ventricular hypertrophy, and expression of TGF-β1 and TGF-β1-regulated genes were investigated. ACE inhibition reduced blood pressure in all groups. When normalised to blood pressure, a significant reduction in hypertrophy was found in ovariectomised animals receiving E2. Expression of TGF-β1 was increased in all three groups treated with the ACE inhibitor, with top levels in ovariectomised animals. Moreover, expression of ornithine decarboxylase (ODC), an adrenoceptor dependent gene, downstream of TGF-β1, was up-regulated upon ACE inhibition, except in animals which were ovariectomised and oestrogen supplemented. Parathyroid hormone-related peptide, a growth factor negatively regulated by TGF-β1, was down-regulated in all animals receiving the ACE inhibitor.

Conclusion: ACE inhibition modulated TGF-β1 and TGF-β1 dependent genes. Oestrogen deficiency alone did not influence the progression of cardiac hypertrophy in this model of female SHR.

Key Words: Oestrogen • ACE-inhibition • Hypertension • Cardiac hypertrophy • Gene-expression

Received May 25, 2004; Accepted March 3, 2005


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