A comprehensive discussion of the interaction of estrogens with the components of the cardiovascular system is beyond the scope of this book, so only a few well-known examples will be given here. It should be noted that in all these situations, estradiol is acting in a milieu that contains many other hormones and growth factors and therefore is only one of many factors influencing these systems. One physiological importance of the role of E2 in the cardiovascular system in humans lies in the effects of its withdrawal at menopause and the clinical approaches to replacing it following this withdrawal.

One of the most widely studied and best under stood effects of estrogens in the cardiovascular system is vasorelaxation. This is brought about by stimulation of endothelial NO synthase (eNOS) in the endothelial cells. The effects of E2 on the endothelial cell involve nuclear actions of ERα leading to the increased transcription and stability of mRNA for eNOS. In addition, as outlined in Figure 1, E2 acts through rapid membrane initiated events. Studies of the latter effects have implicated ERα and/or ERβ located in caveolae of the plasma membrane, which activates the PI3K/Akt pathway leading to phosphorylation of eNOS at S1177. E2-mediated activation of EGF (epidermal growth fac tor) also stimulates eNOS phosphorylation and thus vasodilation. It should be noted that enzymes that affect the local concentrations of active E2, such as aromatase, are also located in vascular endothelial cells.

Fig1. Mechanism of E2-mediated vasodilation in vascular endothelial cells. The model depicts the interaction of E2 with a subpopulation of ERα that resides in the plasma membrane. The hormone-ER complex interacts with intracellular proteins, such as c-Src, a non-receptor tyrosine kinase, which can activate the PI3 kinase pathway or, through EGFR (epidermal growth factor receptor), the MAP kinase pathway. The result is the activation of eNOS by phosphorylation of serine-1177, which through the NO/cGMP pathway results in vasodilation.

Other effects of E2 on the cardiovascular system include its inhibition of vascular smooth muscle (VSMC) proliferation, particularly in response to hyperglycemia. E2 also exerts a protective effect on the heart by inhibiting apoptosis and necrosis of myocardial cells. Following a myocardial infarction, E2 pro motes restorative cardiac remodeling and angiogenesis. Many studies suggest that these cardioprotective effects are mediated by ERβ. Finally, E2, by increasing expression of genes for antioxidants, helps protect the vasculature against the damage done by reactive oxygen species (ROS).

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مواضيع ذات صلة

Polycystic Ovary Syndrome (PCOS)

Effects of Estrogen on Bone

Uterine Effects of Estrogen and Progesterone

Menopause

Chemistry and Metabolism of Female Steroid Hormones: Feedback Effects on the Hypothalamus and Pituitary

Control of the Ovary by the Hypothalamus and Pituitary

Synthesis of Progesterone and Estrogens

Female Steroid Hormones

The Androgen Receptor

Hypothalamic-Pituitary-Testis Axis: Feedback Control

Causes of Destructive (Low RAIU) Thyrotoxicosis

Causes of Hyperthyroidism