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17α-ethinylestradiol modulates endothelial function in ovariectomized rat carotid arteries
Fang Yuan1, Satoshi Obayashi2, Ayumi Yamaguchi1
1Department of Comprehensive Reproductive Medicine, Graduate School, Tokyo Medical & Dental University, Tokyo, Japan.
European Journal of Pharmacology
|February 5, 2023
Summary
17α-ethinylestradiol (EE2) enhances endothelial function but has a weaker ability to produce nitric oxide (NO) than 17β-estradiol (E2). EE2 also uniquely increases endothelial-derived hyperpolarizing factor activity.
Area of Science:
- Endocrinology
- Cardiovascular Research
- Pharmacology
Background:
- 17α-ethinylestradiol (EE2), a synthetic estrogen in oral contraceptives, is linked to cardiovascular risks.
- Endothelial dysfunction is a key factor in cardiovascular events.
- Limited research exists on EE2's specific effects on endothelial function.
Purpose of the Study:
- To investigate the impact of EE2 on endothelial function in ovariectomized rats.
- To compare the endothelial effects of EE2 with 17β-estradiol (E2).
- To elucidate the mechanisms underlying EE2-mediated endothelial responses.
Main Methods:
- Ovariectomized rats were treated with EE2, E2, or a control.
- Vascular endothelial function was assessed via acetylcholine-induced relaxation.
- Endothelial nitric oxide synthase (eNOS) expression and arterial structure were analyzed.
Main Results:
- Both EE2 and E2 treatments improved endothelium-dependent relaxation.
- EE2 treatment showed higher eNOS expression than controls but lower than E2.
- EE2 enhanced endothelial-derived hyperpolarizing factor activity, unlike E2.
Conclusions:
- EE2 improves endothelial function, partly through mechanisms independent of nitric oxide production.
- EE2 exhibits a diminished capacity for nitric oxide generation compared to E2.
- EE2 uniquely augments endothelial-derived hyperpolarizing factor activity, suggesting a distinct endothelial signaling pathway.
