Key result
Menopause and estrogen deficiency alter central autonomic regulation and enhance vascular adrenergic sensitivity, potentially elevating resting blood pressure and pressor responses to stress.
The review highlights that estrogen deficiency in menopause leads to increased sympathetic nerve activity and vascular adrenergic sensitivity, contributing to the pathogenesis of hypertension in postmenopausal women.
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May inform BP strategies in postmenopausal women; leaves open whether autonomic-targeted interventions improve outcomes.
A large body of evidence indicates a major influence of sex hormones, particularly estrogen, on autonomic regulation of blood pressure (BP). The sympathetic nervous system is now widely recognized as a major regulator of BP homeostasis and contributor to pathogenesis of hypertension in humans. Menopause is accompanied by an accelerated age-related rise in sympathetic nerve activity (SNA). Mechanisms underlying sympathetic activation in menopause are unknown but may be related to impaired central modulation of baroreflex function or direct inhibitory influence of estrogen on SNA. Menopause is also accompanied by enhanced alpha-adrenergic peripheral vasoconstriction both at rest and during exercise. In ovariectomized rats, reduced nitric oxide release from the skeletal muscle caused by estrogen deficiency contributes to augmented sympathetic vasoconstriction during muscle contraction. The alteration in central autonomic regulation coupled with enhanced vascular adrenergic sensitivity may be responsible for elevation in resting BP and exaggerated pressor responses to exercise and mental stress in postmenopausal women.
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Wanpen Vongpatanasin (2009) conducted a review in Menopause and blood pressure regulation. Menopause was evaluated. Menopause and estrogen deficiency alter central autonomic regulation and enhance vascular adrenergic sensitivity, potentially elevating resting blood pressure and pressor responses to stress.
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