Key result
Older postmenopausal status is linked to blunted beta-2-mediated vasodilation compared with premenopausal women.
Why the study?
The role of β2AR vasodilatation and nitric oxide contribution in hypertension pathophysiology in ageing postmenopausal women was unclear.
Does postmenopausal status and aging reduce beta-2-adrenergic receptor-mediated forearm vasodilatation and nitric oxide contribution in women?
Cross-Sectional (n=21)
No
Does postmenopausal status and aging reduce beta-2-adrenergic receptor-mediated forearm vasodilatation and nitric oxide contribution in women?
These findings indicate that aging and postmenopausal status are associated with blunted beta-2-adrenergic receptor responsiveness and diminished nitric oxide contribution, which may predispose postmenopausal women to hypertension and cardiovascular disease.
May heighten hypertension risk in postmenopausal women; hypothesis-generating for β2-adrenergic mechanisms in vascular aging.
New Findings What is the central question of this study? What is the role of β 2 ‐adrenergic receptor (β 2 AR) vasodilatation in older postmenopausal women as compared to premenopausal women and the role of nitric oxide (NO) in β 2 AR‐mediated vasodilatation in both groups of women? What is the main finding and its importance? β 2 AR responsiveness is blunted in postmenopausal women compared to young premenopausal women. Additionally, NO may contribute to β 2 AR‐mediated vasodilatation in young premenopausal women. Abstract β 2 ‐Adrenergic receptor (β 2 AR)‐mediated vasodilatation, which is partially dependent on nitric oxide (NO) formation, is blunted in men at risk for developing hypertension. However, the role of β 2 AR vasodilatation in hypertension pathophysiology in ageing postmenopausal women is unclear. Therefore, the goals of this study were to determine if forearm vasodilatation to the selective β 2 AR agonist terbutaline is blunted in older postmenopausal women (59 ± 4 years) compared to young premenopausal women (27 ± 3 years) and to assess NO contribution to β 2 AR‐mediated vasodilatation in both groups of women. Forearm blood flow (FBF) and forearm vascular conductance (FVC) were measured using venous occlusion plethysmography at baseline and during intra‐arterial infusions of terbutaline at 0.1–2.0 µg (100 ml tissue) −1 min −1 with and without the NO synthase inhibitor l ‐ N G ‐monomethylarginine ( l ‐NMMA). Mean arterial pressure was significantly greater in postmenopausal women than in young women at baseline ( P = 0.01). Baseline FBF and FVC did not differ between young and postmenopausal women ( P > 0.05) and rose significantly within each group during terbutaline infusion ( P < 0.05). There were significant group × dose interactions for FBF ( P = 0.01) and FVC ( P = 0.001), indicating vasodilator responses were lower in postmenopausal women. In young women, FVC response to the highest dose of terbutaline tended to be lower with l ‐NMMA co‐infusion vs . without l ‐NMMA ( P = 0.05). There were no significant decreases in FBF or FVC responses to terbutaline in postmenopausal women with l ‐NMMA co‐infusion ( P > 0.05 for all). These data suggest that β 2 AR responsiveness is blunted in postmenopausal women compared to young premenopausal women, and that NO may contribute to β 2 AR‐mediated vasodilatation in young premenopausal women.
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Harvey et al. (2020) conducted a cross-sectional in Healthy (free of cardiovascular disease) (n=21). Postmenopausal status vs. Young premenopausal status was evaluated on Forearm blood flow (FBF) and forearm vascular conductance (FVC) responses to terbutaline infusion (p=0.01). Older postmenopausal women had significantly blunted forearm vasodilator responses to the selective beta-2-adrenergic receptor agonist terbutaline compared to young premenopausal women (group x dose interaction P=0.01 for FBF).
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