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Vascular Aging across the Menopause Transition in Healthy Women

DOI: 10.1155/2014/204390

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Abstract:

Vascular aging, featuring endothelial dysfunction and large artery stiffening, is a major risk factor for developing cardiovascular disease (CVD). In women, vascular aging appears to be accelerated during the menopause transition, particularly around the late perimenopausal period, presumably related to declines in ovarian function and estrogen levels. The mechanisms underlying endothelial dysfunction and large artery stiffening with the menopause transition are not completely understood. Oxidative stress and the proinflammatory cytokine tumor necrosis factor-α contribute to endothelial dysfunction and large artery stiffening in estrogen-deficient postmenopausal women. Habitual endurance exercise attenuates the age-related increase in large artery stiffness in estrogen-deficient postmenopausal women and can reverse arterial stiffening to premenopausal levels in estrogen-replete postmenopausal women. In contrast, estrogen status appears to play a key permissive role in the adaptive response of the endothelium to habitual endurance exercise in that endothelial improvements are absent in estrogen-deficient women but present in estrogen-replete women. We review here the current state of knowledge on the biological defects underlying vascular aging across the menopause transition, with particular focus on potential mechanisms, the role of habitual exercise in preserving vascular health, and key areas for future research. 1. Introduction Despite significant declines in cardiovascular disease (CVD) mortality, CVD is still the leading cause of death in adults [1]. Vascular aging, featuring endothelial dysfunction and large artery stiffening, is a major risk factor for the development of CVD, in that it combines with other known risk factors to create an age-disease interaction [2]. In women, vascular aging is unique in that adverse changes in CVD risk factors (e.g., blood pressure, lipids, and adiposity) occur during a time of profound changes in the hormonal environment as women transition through menopause. The acceleration of age-associated declines in vascular function in women after menopause suggests that menopause may be a triggering event that leads to increased vascular vulnerability as women age. Thus, understanding the underlying biological defects associated with vascular aging across the menopause transition is important for the development of strategies to maintain vascular health and decrease CVD mortality. This review will focus on some of the work that we have done on the modulatory influence of sex hormone deficiency on vascular aging in

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