Before menopause, high blood pressure is not a high risk factor for most women. But after menopause hypertension can become a rather serious issue. Certain factors contributing to this development have been discussed in a recent review (Am J Hypertens. 2011 Jul; 24(7):740-9). For women in their reproductive years, higher estradiol levels are believed to be protective against high blood pressure. Estradiol helps keep blood vessels flexible.
Researchers have discovered that pre-menopausal women have a lower systolic and diastolic pressure than men, but it increases in post-menopausal women as much as 5 mmHg. As the estradiol and progesterone levels continue to decrease, causing estrogen dominance, the post-menopausal woman is more at risk of developing high blood pressure than the man. While antihypertensive methods are similar between men and women and women are more likely to have their blood pressure measured, hypertension may be less well controlled in women. This suggests that perhaps the mechanisms responsible for hypertension in women may differ from the mechanisms in men.
Cardiovascular disease is the leading cause of morbidity and mortality in postmenopausal women. Hypertension is a major risk factor for cardiovascular disease. The mechanisms responsible for postmenopausal hypertension have not been completely elucidated. However, various mechanisms have been implicated. For example, there is evidence that changes in the estrogen/androgen ratios favoring increased androgens, activation of the renin-angiotensin and endothelin systems, activation of the sympathetic nervous system, metabolic syndrome and obesity, inflammation, increased vasoconstrictor eicosanoids, and anxiety and depression may be important in the pathogenesis of postmenopausal hypertension. There is also evidence that hypertension is less well controlled in aging women than in aging men, but the reasons for this gender difference is not clear. Postmenopausal hypertension is likely multifactorial.
Several physiological systems have been implicated in clinical studies. For example, postmenopausal women exhibit increases in plasma renin activity and endothelin, compared to their premenopausal counterparts. Longitudinal studies have shown that serum androgen levels are increased in postmenopausal women, leading to alterations in estrogen/androgen ratios. In addition, it has been reported that hypertension in postmenopausal women, not age-matched men, was associated with elevated excretion of 20-hydroxyeicosatetraenoic acids (20-HETE), vasoconstrictor eicosanoids.
Markers of oxidative stress are also increased in postmenopausal women, and oxidative stress has been shown to increase BP by reducing the bioavailability of nitric oxide (NO). The incidence of obesity may be as high as 40% in postmenopausal women, and increases in body weight have been shown to be associated with increases in BP. Obesity is one component of the cluster of features known as the metabolic syndrome that also includes insulin resistance, type 2 diabetes, hyperlipidemia, and hyperleptinemia, that could also impact BP.
Chronic inflammation and increased levels of cytokines have been shown to contribute to hypertension in certain circumstances, such as in models of pre-eclampsia. Although inflammation and inflammatory cytokines are elevated with menopause, the role that chronic inflammation plays in mediating postmenopausal hypertension is not clear. In addition to having a direct effect on BP, inflammation may also be a consequence of lack of psychological well-being in these aging women.
In experimental settings, many in vitro, estradiol has been shown to have a variety of effects that should be protective of cardiovascular health. Proponents of the beneficial role of estradiol in cardiovascular disease cite the use of progesterone in HRT as possibly negating the positive effects of estradiol. However, in women with surgical menopause and hysterectomy, estrogen replacement therapy alone, does not result in significant sustained reductions in blood pressure or reductions in cardiovascular disease risk. Thus, reductions in estradiol that occur at menopause do not fully explain the progressive increases in blood pressure in postmenopausal women, and estrogen replacement is not used as an antihypertensive in their treatment.
There is evidence though that loss of estrogens (remember there are multiple endogenous estrogens) at any age contributes to endothelial dysfunction, which is common in individuals with hypertension.Authors hypothesize that change in estrogen/androgen ratios that favor increases in androgens lead to activation of the renin–angiotensin system (RAS). Increases in androgens can increase endothelin levels, and subsequently increase ω-hydroxylase activity (and 20-HETE synthesis) by increasing release of arachidonic acid from plasma membranes. Androgens promote increase in vascular 20-HETE. Authors also suggest that the increases in androgens with aging in postmenopausal women leads to increases in food intake and visceral adiposity. This then leads to increases in leptin, which in turn activate the sympathetic nervous system via the melanocortin 4 receptors in the hypothalamus. The combination of reductions in estrogens, increases in androgens, increases in visceral adiposity lead to increases in inflammatory cytokines, such as TNF-α.
Further studies are necessary to delineate the mechanisms responsible for postmenopausal hypertension and to develop treatment options specific for women. But general recommendations are clear and simple. To control your blood pressure both before and after menopause, focus on a healthy lifestyle:
• Maintain a healthy weight.
• Eat heart-healthy foods, such as whole grains, fruits and vegetables.
• Reduce the amount of salt in your diet.
• Exercise on most days of the week.
• Limit or avoid alcohol.
• If you smoke, stop.