Key result
Estrogen is hypothesized to modulate cardiac natriuretic peptides in females by affecting the renin-angiotensin system directly or indirectly, potentially explaining its cardioprotective effects.
This review highlights the hypothesis that estrogen's cardioprotective effects may be mediated through modulation of natriuretic peptides and the renin-angiotensin system.
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Non-lipid mechanisms likely mediate remaining estrogen cardioprotection; leaves open targeted mechanistic studies in premenopausal women.
There are significant gender-specific differences in the incidence of hypertension and the clinical outcome of cardiovascular disease between premenopausal women and age-matched men, suggesting that sex hormones such as estrogen (E) might be responsible for the observed cardioprotective effects. This cardioprotective action of E is thought to involve lipoproteins. However, the effect of E on the lipid profile accounts for about 50% of the reduction in cardiovascular disease, indicating that there might be other mechanisms by which E exerts its cardioprotective effects. At present, the underlying mechanism of E action is poorly understood. In this review, the interplay between E, the natriuretic peptides (NP) and the renin-angiotensin system (RAS) is examined. It is hypothesized that E might, through endocrine and/or paracrine action, modulate cardiac NP in females by affecting the RAS either directly or indirectly.
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Mercedes L. Kuroski de Bold (1999) conducted a review in Cardiovascular disease and hypertension. Estrogen was evaluated. Estrogen is hypothesized to modulate cardiac natriuretic peptides in females by affecting the renin-angiotensin system directly or indirectly, potentially explaining its cardioprotective effects.
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