Why the study?
Does ACE inhibition with moexiprilat interact with oestrogen status to reduce left ventricular hypertrophy in female spontaneously hypertensive rats?
Does ACE inhibition with moexiprilat interact with oestrogen status to reduce left ventricular hypertrophy in female spontaneously hypertensive rats?
In female spontaneously hypertensive rats, ACE inhibition reduces blood pressure, but its ability to reduce cardiac hypertrophy is significantly enhanced by estrogen replacement.
Answers are grounded in this paper and cite their sources.
Estrogen may enhance ACEi effects on hypertrophy beyond BP reduction in rats; leaves open translation to human hypertension.
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)-beta(1) in female spontaneously hypertensive rats (SHR). METHODS AND RESULTS: Intact female SHR, ovariectomised SHR, and ovariectomised SHR with 17beta-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(1)-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(1) 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(1) and TGF-beta(1) dependent genes. Oestrogen deficiency alone did not influence the progression of cardiac hypertrophy in this model of female SHR.
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Martin et al. (2005) studied this question.
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