Abstract

Reproductive hormones have important non‐reproductive influences on cardiovascular structure and function. In women, these include important effects on the autonomic control of the circulation. Women under the age of 40 tend to have less tonic activity of sympathetic vasoconstrictor nerves in the periphery (usually measured as muscle sympathetic nerve activity), as well as smaller hearts and lower cardiac output compared to men of similar age and health status. Together, these result in a tendency for lower blood pressures in young women, including decreased risk for hypertension, and increased risk of hypotensive disorders such as orthostatic intolerance. Female reproductive hormones (particularly estrogen) appear to contribute to increased functional activity of vascular beta‐2 adrenergic receptors, which offset alpha‐adrenergic vasoconstriction and result in less vasoconstriction for a given amount of sympathetic neural activity (or local norepinephrine), also contributing to the lower blood pressure in young women compared to young men. At menopause, the influences of the hormones decreases, and sex differences are minimized or reversed: sympathetic nerve activity and blood pressure increase to levels similar to, or higher than, those seen in older men. The vasodilator influence of beta‐2 receptors decreases, and sympathetic nerve activity becomes more tightly linked to vasoconstriction and blood pressure. Sympathetic neural activity thus becomes a greater contributor to blood pressure with aging in both men and women, and is a factor in the increased risk of hypertension in older age in both sexes.Support or Funding InformationFunded by USAMRMC; author views not official US Army or DOD policyThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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