Acute exogenous oestradiol augments endothelial and smooth muscle vasodilatory responsiveness in premenopausal but not postmenopausal females.

Abstract

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 β₂-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 (β₂-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. 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.