Estrogen and the cardiovascular system

Abstract

Estrogen is a potent steroid with pleiotropic effects, which have yet to be fully elucidated. Estrogen has both nuclear and non-nuclear effects. The rapid response to estrogen, which involves a membrane associated estrogen receptor(ER) and is protective, involves signaling through PI3K, Akt, and ERK 1/2. The nuclear response is much slower, as the ER-estrogen complex moves to the nucleus, where it functions as a transcription factor, both activating and repressing gene expression. Several different ERs regulate the specificity of response to estrogen, and appear to have specific effects in cardiac remodeling and the response to injury. However, much remains to be understood about the selectivity of these receptors and their specific effects on gene expression. Basic studies have demonstrated that estrogen treatment prevents apoptosis and necrosis of cardiac and endothelial cells. Estrogen also attenuates pathologic cardiac hypertrophy. Estrogen may have great benefit in aging as an anti-inflammatory agent. However, clinical investigations of estrogen have had mixed results, and not shown the clear-cut benefit of more basic investigations. This can be explained in part by differences in study design: in basic studies estrogen treatment was used immediately or shortly after ovariectomy, while in some key clinical trials, estrogen was given years after menopause. Further basic research into the underlying molecular mechanisms of estrogen’s actions is essential to provide a better comprehension of the many properties of this powerful hormone.

The Effect of Cardiovascular Responses after Aerobic Exercise in Menstrual Cycle

“…Decreased estrogen levels during menstruation influence an increase of peripheral resistance as the sympathetic nervous system is more activated and peripheral blood vessels are more contracted [1]. At ovulation, increased estrogen levels not only affect vascular relaxation by triggering the activation of nitric oxide, the vascular relaxant factor, but also are attributable to a lower blood pressure during exercise than at menstruation by having a direct relaxant effect on the smooth muscles [19].…”

“…Low estrogen levels during menstruation typically result in contraction of peripheral blood vessels by activating the sympathetic nervous system [1]. In addition, norepinephrine levels, an indicator of sympathetic activity, are higher in the menstruation phase than in the ovulation phase [20].…”

“…Menopause intensifies the risk of cardiovascular disease drastically in women compared with men of the same age by increasing low-density lipoprotein cholesterol (LDLC) levels and blood pressure [1]. For this reason, measures have been devised in attempts to improve and prevent cardiovascular disease in women, and of these, participation in physical activity is the most effective and recommended option [2].…”

“…Changes in women's hormone levels during exercise induce differences in physiological responses [1]. Increasing blood pressure is a cardiovascular response to exercise as workout intensity increases, followed by rises in heart rate (HR) and stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) [4].…”

“…Reduction in estrogen secretion during menstruation activates the sympathetic nervous system and this can lead to vascular contraction by increasing sensitivity to norepinephrine and α-adrenergic receptors and excessive blood pressure response during exercise by increasing TPR [1] [7]. On the contrary, raised estrogen levels in the ovulatory phase lower blood pressure during exercise by inducing vascular relaxation through activation of nitric oxide which is a vascular relaxant factor produced by vascular endothelial cells [7].…”