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Cardiac norepinephrine release: modulation by ovariectomy and estrogen
Bernard A Eskin1, David L Snyder, Jay Roberts
1Department of Obstetrics, Drexel University College of Medicine, Philadelphia, Pennsylvania 19129, USA. bae22@drexel.edu
Experimental Biology and Medicine (Maywood, N.J.)
|February 4, 2003
Summary
Estrogen depletion via ovariectomy increases norepinephrine release from rat heart nerve terminals. Estrogen replacement therapy restores normal release, suggesting a protective role for estrogen in cardiac synapses.
Area of Science:
- Cardiovascular Physiology
- Neuroendocrinology
- Pharmacology
Background:
- Female rats do not exhibit age-related decreases in cardiac norepinephrine release, unlike males.
- Sex hormones, particularly estrogen, may influence norepinephrine release from female rat cardiac synaptosomes.
Purpose of the Study:
- To investigate how long-term estrogen depletion (ovariectomy) and subsequent estrogen replacement affect norepinephrine release from cardiac synaptosomes.
- To test if estrogen modulates depolarization-elicited norepinephrine release in female rats.
Main Methods:
- Female F344 rats underwent ovariectomy or sham surgery.
- Ovariectomized rats received conjugated equine estrogens, delta8,9-dehydroestrone, or 17 alpha-dihydroequilenin, or vehicle.
- Cardiac synaptosomes were isolated and tested for norepinephrine release after 90 or 270 days.
- Ovariectomy effectiveness was confirmed via vaginal smears, uterine weights, and serum LH levels.
Main Results:
- Ovariectomy significantly increased depolarization-induced norepinephrine release at both 90 and 270 days.
- Estrogen treatments normalized norepinephrine release in ovariectomized rats.
- Long-term conjugated estrogen treatment (270 days) reduced release below sham levels.
Conclusions:
- Estrogen plays a significant role in modulating depolarization-elicited norepinephrine release from cardiac nerve terminals.
- Estrogen's modulation of norepinephrine release may offer a protective effect at the cardiac synapse.