Key result
Acute 17β-estradiol infusion augments microvascular vasodilation in premenopausal but not postmenopausal women.
Why the study?
Menopause is associated with vascular dysfunction as endogenous oestradiol concentrations diminish, but the effect of acute exogenous oestradiol on specific vasodilatory pathways in females remained to be determined.
Does acute exogenous 17β-oestradiol augment endothelium-dependent, endothelium-independent, and β2-adrenergic receptor-induced vasodilatation in premenopausal and postmenopausal females?
Does acute exogenous 17β-oestradiol augment endothelium-dependent, endothelium-independent, and β2-adrenergic receptor-induced vasodilatation in premenopausal and postmenopausal females?
Acute exogenous oestradiol improves microvascular vasodilatation in premenopausal but not postmenopausal females, suggesting a loss of vascular responsiveness to oestradiol after menopause.
Supports menopause-associated loss of microvascular oestradiol responsiveness; hypothesis-generating for cardiovascular risk in aging females.
Menopause is associated with vascular dysfunction. During the menopausal transition, endogenous oestradiol concentrations diminish. Oestradiol is vasoprotective because it has direct and indirect effects on the vasculature. The present study aimed to determine the effect of acute exogenous oestradiol on endothelium‐dependent, endothelium independent and β 2 ‐adrenergic receptor‐induced vasodilatation in females. Forearm blood flow (venous occlusion plethysmography) was measured during brachial intraarterial infusions of ACh (endothelium‐dependent agonist), sodium nitroprusside (endothelium independent agonist) and terbutaline (β 2 ‐adrenergic receptor agonist) with and without concurrent infusion of 17β‐oestradiol. Nine young premenopausal (age: 26 ± 4 years) and nine postmenopausal (PM, age: 58 ± 4 years, 8 ± 1 years post‐menopause) females completed the study. Concurrent oestradiol infusion augmented the vasodilatory response to ACh, sodium nitroprusside and terbutaline in young premenopausal (all P < 0.05) but not older postmenopausal (all P > 0.05), females. Local infusion of exogenous 17β‐oestradiol augmented endothelial and smooth muscle microvascular vasodilatation in premenopausal but not postmenopausal, females. image Key points Menopause is associated with vascular dysfunction. Because oestradiol has vasoprotective effects, the menopause‐associated drop in oestradiol concentrations is hypothesized to contribute to vascular dysfunction during the menopause transition. The present study shows that local infusion of exogenous oestradiol augmented microvascular vasodilatation in premenopausal but not postmenopausal females.
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Dillon et al. (2025) studied Menopause (n=18). 17β-oestradiol vs. Without concurrent infusion of 17β-oestradiol was evaluated on Vasodilatory response to ACh, sodium nitroprusside and terbutaline (p=<0.05). Acute local infusion of exogenous 17β-oestradiol augmented endothelial and smooth muscle microvascular vasodilatation in premenopausal (P<0.05) but not postmenopausal females (P>0.05).
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