Women's health — why does nitric oxide protect women's hearts differently?

Aim of the study: Sex differences are widely recognized as a key risk factor for cardiovascular disease (CVD). Estrogen, the primary female sex hormone, improves cardiovascular function through genomic or non-genomic mechanisms initiated by receptors (ERα, ERβ, or G protein-coupled estrogen receptor).

Results: Estrogen, the primary female sex hormone, improves cardiovascular function through genomic or non-genomic mechanisms initiated by receptors (ERα, ERβ, or G protein-coupled estrogen receptor). Gaseous signaling molecules, including nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO), are important regulators of cardiovascular function. Recent studies have shown that estrogen regulates the production of these signaling molecules in cardiovascular cells, producing protective effects on the cardiovascular system. We discuss current understanding of gaseous signaling molecules in cardiovascular disease (CVD), the mechanisms by which estrogen provides cardiovascular protection by regulating these molecules, and how these findings can be applied to improve the health of postmenopausal women.

Aim of the study: There are considerable sex differences in the risk of cardiovascular disease (CVD), including arterial hypertension, coronary artery disease (CAD), and stroke, as well as chronic kidney disease. Women are largely protected from these conditions before menopause, and the risk increases after natural estrogen production stops or following surgical menopause.

Results: Estrogens improve the widening of the large coronary arteries and the coronary microvasculature by increasing the release of vasodilating factors such as nitric oxide and prostacyclin. These mechanisms of coronary artery dilation are more pronounced in women than in men. Estrogens are also powerful inhibitors of inflammation, which partly explains their protective effects against CVD and chronic kidney disease. Emerging evidence suggests that sex chromosomes also play a significant role in shaping cardiovascular risk. The cardiovascular protection provided by natural estrogens may be extended by hormone therapy, especially with bioidentical hormones and when treatment starts early after menopause.

Aim of the study: Cardiovascular disease is the leading cause of death in women and claims the lives of more than half a million women every year. High blood pressure is one of the most common and powerful contributors to atherosclerotic cardiovascular disease.

Results: However, little information is available on the effects of HRT on blood pressure in hypertensive postmenopausal patients. The heart-protective effects of estrogens are not fully understood, but they may involve direct effects on blood vessels through changes in natural vasoconstrictors and vasodilators, as well as reductions in blood lipoprotein and cholesterol levels. Experimental evidence suggests that estrogen increases the biological effects of nitric oxide and decreases the effects of angiotensin. After menopause, the loss of estrogen's protective effects on blood vessels may reveal a group of women who are especially prone to high blood pressure and therefore at higher risk for cardiovascular disease.

Aim of the study: Menopause is not a disease, but a normal phase in a woman's life caused by changes in hormone levels. Difficult symptoms may be associated with changes in metabolism, along with new cardiovascular risk factors that can be particularly harmful to the female cardiovascular system, which has been protected during the fertile years.

Results: Postmenopause is also often associated with high blood pressure, the factor most commonly linked to coronary artery disease. High blood pressure is associated with increased body mass index, insulin resistance, sodium retention, increased blood viscosity, and estrogen deficiency, which increases the growth of smooth muscle cells and raises systemic vascular resistance. Age and estrogen deficiency together are the most important causes of cardiovascular risk after menopause. The discovery of alpha and, more recently, beta estrogen receptors on coronary vessels in women without atherosclerosis, both before and after menopause, may help explain the causes of coronary artery disease in women and has important implications for treatment.