Journalartikel

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


Autorenlistevan Eickels, M; Schreckenberg, R; Doevendans, PA; Meyer, R; Grohé, C; Schlüter, KD

Jahr der Veröffentlichung2005

Seiten1079-1084

ZeitschriftEuropean Journal of Heart Failure

Bandnummer7

Heftnummer7

ISSN1388-9842

eISSN1879-0844

DOI Linkhttps://doi.org/10.1016/j.ejheart.2005.03.004

VerlagWiley


Abstract

Background: ACE inhibitors are widely used to antagonize the biological activity of angiotensin IT in hypertensive heart disease. Oestrogen reduces angiotensin type I 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)-beta(1) in female spontaneously hypertensive rats (SHR).

Methods and results: Intact female SHR, ovariectomised SHR, and ovariectomised SHR with 17 beta-oestradiol (E2) replacement therapy were either treated with placebo or the ACE inhibitor moexiprilat. Blood pressure, left ventricular hypertrophy, and expression of TGF-beta(1) and TGF-beta -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-beta 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-beta(1) 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-beta(1), was down-regulated in all animals receiving the ACE inhibitor.

Conclusion: ACE inhibition modulated TGF-beta and TGF-beta dependent genes. Oestrogen deficiency alone did not influence the progression of cardiac hypertrophy in this model of female SHR. (c) 2005 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.




Zitierstile

Harvard-Zitierstilvan Eickels, M., Schreckenberg, R., Doevendans, P., Meyer, R., Grohé, C. and Schlüter, K. (2005) The influence of oestrogen-deficiency and ACE inhibition on the progression of myocardial hypertrophy in spontaneously hypertensive rats, European Journal of Heart Failure, 7(7), pp. 1079-1084. https://doi.org/10.1016/j.ejheart.2005.03.004

APA-Zitierstilvan Eickels, M., Schreckenberg, R., Doevendans, P., Meyer, R., Grohé, C., & Schlüter, K. (2005). The influence of oestrogen-deficiency and ACE inhibition on the progression of myocardial hypertrophy in spontaneously hypertensive rats. European Journal of Heart Failure. 7(7), 1079-1084. https://doi.org/10.1016/j.ejheart.2005.03.004



Schlagwörter


ACE-inhibitionCardiac hypertrophyCARDIAC-HYPERTROPHYHEART-FAILUREoestrogenORNITHINE-DECARBOXYLASEPTHRPTGF-BETA EXPRESSION

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