Key result
Transdermal estrogen linked to increased VEGF and PGE2 and lower SBP in normotensive postmenopausal women.
Why the study?
Does transdermal estrogen therapy affect vasoactive humoral factors and ambulatory blood pressure in normotensive postmenopausal women?
Does transdermal estrogen therapy affect vasoactive humoral factors and ambulatory blood pressure in normotensive postmenopausal women?
Transdermal estrogen therapy increases vasodilatory factors VEGF and prostaglandin E2 and reduces systolic blood pressure in normotensive postmenopausal women, suggesting a potential mechanism for cardiovascular benefit.
Transdermal estrogen was associated with higher VEGF/PGE2 and lower SBP; leaves open whether these changes affect cardiovascular outcomes.
BACKGROUND: Mechanisms of the vasoprotective effect of hormone replacement therapy (HRT) are not completely understood, and they may involve direct actions on blood vessels through modulation of endogenous vasoconstrictors and vasodilators. Most studies have focused on estrogen action on prostacyclin and nitric oxide, while insufficient data exist concerning the effect of estrogen replacement therapy (ERT) on vascular endothelial growth factor (VEGF) and prostaglandin E(2). OBJECTIVE: The aim of this study was to examine the effect of transdermal estrogen therapy on VEGF, prostaglandin E(2) and active renin in normotensive postmenopausal women. METHODS: Transdermal estrogen (Climara) (Schering): 50 microg 17beta-estradiol) was given for 3 months to normotensive women with a surgically induced menopause, and serum levels of VEGF, active renin and prostaglandin E(2) were measured before and after treatment. In addition, 24-h ambulatory blood pressure monitoring was carried out to determine the estrogen action on mean diurnal and nocturnal systolic and diastolic blood pressure levels. RESULTS: Estradiol treatment resulted in a significant increase in both VEGF and prostaglandin E(2). There was no significant change in active renin levels. However, out-patient monitoring showed a significant fall in systolic blood pressure (daytime, night-time and total 24-h). The stimulating action of ERT on VEGF and prostaglandin E(2) suggests that both factors can elicit estrogen vasodilatory effects. CONCLUSION: The estrogen-mediated increase in serum VEGF and prostaglandin E(2) concentrations may be a mechanism by which HRT benefits the cardiovascular system.
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Zacharieva et al. (2002) studied Normotensive postmenopausal women. Transdermal estrogen (17beta-estradiol) vs. Baseline (before treatment) was evaluated on Serum levels of VEGF, active renin, prostaglandin E2, and 24-h ambulatory blood pressure. Transdermal estrogen therapy for 3 months significantly increased serum VEGF and prostaglandin E2 and decreased systolic blood pressure in normotensive postmenopausal women.
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