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Postmenopausal Estrogen Administration Suppresses Muscle Sympathetic Nerve Activity¹

Department of Internal Medicine I (G.W., J.B., H.L.F., C.D.), Medical University Lübeck, 23538 Lübeck, Germany; and Department of Clinical Neurophysiology (M.E.), University of Göteborg, S-41345 Göteborg, Sweden

Address correspondence and requests for reprints to: Christoph Dodt, M.D., Department of Internal Medicine, Medical University Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany. E-mail: dodt{at}medinf.mu-luebeck.de

The activity of the sympathetic nervous system shows gender-specific differences with lower sympathoneural activity to the muscle vascular bed in women compared with men, with this difference vanishing after menopause. The present study tested the hypothesis that estrogen exerts regulatory influence on the autonomic nervous system in postmenopausal women. Eleven healthy postmenopausal women (age, 58.5 ± 1.0 yr; mean ± SEM) were studied in a randomized double-blind crossover protocol with transdermal administration of 100 µg/day estradiol (E₂) or placebo (P) for 2 days. Muscle sympathetic activity (MSA), blood pressure, and heart rate were recorded at rest and during sympathoexcitatory maneuvers (apnea, cold pressor test). E₂ administration significantly increased serum E₂ to physiological levels (E₂, 469.5 ± 51.5; P, 34.8 ± 2.2 pmol/L; P < 0.05) and significantly lowered MSA (E₂, 30.1 ± 3.0 vs. P 37.7 ± 3.1 bursts/min; P < 0.05). At the same time, blood pressure and heart rate were not affected. MSA was significantly enhanced during apnea and the cold pressure test, and this physiological response to the maneuvers was not changed after estrogen supplementation. In conclusion, elevation of low postmenopausal estrogen levels to physiological premenopausal levels by transdermal E₂ administration supresses MSA. This effect is most likely the consequence of a direct E₂ effect on central nervous autonomic centers, which could explain the gender-specific differences in sympathetic outflow to the muscle vascular bed. The sympathoinhibitory estrogen effects could be important for beneficial cardiovascular effects of estrogen replacement therapy in postmenopausal women.

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