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Estrogen increases endothelial nitric oxide by a receptor-mediated system
1Department of Geriatrics, Nagoya University School of Medicine, Japan.
Biochemical and Biophysical Research Communications
|September 25, 1995
Summary
Estrogen enhances endothelial nitric oxide synthase (NOS-3) activity and nitric oxide (NO) release through a receptor-mediated pathway. This effect is diminished by cell senescence, highlighting the role of estrogen receptors in NO production.
Area of Science:
- Cardiovascular Biology
- Endocrinology
- Molecular Biology
Background:
- Atherosclerosis is a major cardiovascular disease.
- Estrogen is known to have protective effects against atherosclerosis.
- The precise mechanism of estrogen's antiatherosclerotic action requires further elucidation.
Purpose of the Study:
- To investigate the mechanism by which estrogen exerts its antiatherosclerotic effects.
- To determine the impact of estrogen on endothelial nitric oxide synthase (NOS-3) activity and nitric oxide (NO) production.
- To explore the role of estrogen receptors in mediating these effects.
Main Methods:
- Primary endothelial cells from human umbilical veins (HUVEC) and bovine aortas (BAEC) were cultured.
- Cells were preincubated with 17 beta-estradiol, and NOS-3 activity was measured.
- Nitric oxide (NO) release was assessed using selective meters and metabolite analysis (NO2-/NO3-).
- Western blot analysis was performed to evaluate NOS-3 levels.
- Estrogen receptor antagonists (tamoxifen, ICI182780) were used to block estrogen's effects.
- Immunocytochemistry was employed to detect estrogen receptor expression in relation to cell passage number.
Main Results:
- 17 beta-estradiol significantly enhanced NOS-3 activity and NO release in HUVEC and BAEC.
- Western blot analysis confirmed that 17 beta-estradiol increased NOS-3 levels.
- Estrogen receptor antagonists blocked the effects of 17 beta-estradiol by approximately 80%.
- The beneficial effects of 17 beta-estradiol diminished in later passage cells (beyond 10th passage).
- Estrogen receptor expression was reduced in senescent BAEC (beyond 16th passage).
Conclusions:
- Estrogen increases endothelial NOS-3 activity and NO release via a receptor-mediated mechanism.
- Estrogen receptors play a crucial role in mediating the release of NO from endothelial cells.
- Cell senescence appears to alter estrogen receptor expression and function, potentially impacting NO production.
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