The incidence of cardiovascular disease in premenopausal women is lower than in men but increases rapidly after the menopause. Oestrogen replacement therapy markedly reduces cardiovascular risk, which can only partially be explained by favourable changes in lipid profile. Recent studies have explored the profound effects of oestrogen on the blood vessel walls. Oestrogens such as 17β-oestradiol cause vascular relaxation by an endothelium-dependent (i.e., stimulation of nitric oxide, inhibition of endothelin-1 production) or -independent mechanism(s) (i.e., calcium antagonist-like effects). Furthermore, 17β-oestradiol stimulates endothelial cell proliferation and migration, whereas it inhibits the proliferation of smooth-muscle cells from animals and humans in vitro, regardless of gender, and inhibits intimal thickening after angioplasty in animal models. 17β- oestradiol also inhibits the production of extracellular matrix components. Therefore, the effects of oestrogen on vascular endothelial and smooth- muscle cells may contribute significantly to the protective role of the hormone in cardiovascular systems in premenopausal women.
|Journal||Journal of Cardiovascular Pharmacology|
|Issue number||SUPPL. 5|
|Publication status||Published - 1996|
- Nitric oxide synthase
- Smooth-muscle cells
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine