Vascular Effects of Estrogens

Blood vessels are complex structures with walls containing smooth muscle cells (SMCs) and an endothelial lining. Far from being only an anatomic barrier, the endothe-lium is a metabolically active organ system that maintains vascular homeostasis by modulating vascular tone, regulating local cellular growth and extracellular matrix deposition and also regulating the hemostatic, inflammatory, and reparative responses to local injury (24).

Vasoregulation occurs as a balance between the release of relaxing and constricting factors. The predominant relaxing factor is nitric oxide (NO), which is synthesized from the amino acid L-arginine. NO release activates SMC guanylate cyclase, leading to increased cyclic guanosine monophosphate production and vascular relaxation (25). Other relaxing factors include prostacyclin and hyperpolarizing factor, which act through cyclic adenosine monophosphate and potassium channels respectively. The major constricting factors are endothelin-1, thromboxane, and prostaglandin H2 (24).

NO synthesis by endothelial cells is of paramount importance for the regulation of vascular tone and blood flow and for control of the hemostatic process. Furthermore, endothelium-derived NO is a potent anti-inflammatory and antiatherogenic factor, being able to prevent endothelial cell dysfunction that has been proposed as an early manifestation of atherosclerosis (26,27).

Estrogen is widely regarded as beneficial to arterial wall function. The beneficial effects include changes in the biology of the endothelium, and the intima-media of the arterial wall. In the arterial endothelium, NO appears to be the primary vascular target of estrogens (28).

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