[Estrogens and the arterial wall]

Two isoforms of oestrogens receptor (alpha and B) have been identified in the cells of the arterial wall, and an heterogenity of their expression according to the animal species, to the vascular bed and to sex has been reported. Estrogens can thus directly influence the vascular physiology through a genomic mechanism, but extra-genomic mechanisms responsible for a short-term effect have also been suggested. Endothelium appears to be an important target for estradiol, because this hormone potentiates endothelium-dependant relaxation through an increase in NO bioavailability, and accelerates endothelial regrowth. In the model of apolipoprotein E-deficient mice, as the atrhroprotective effect deposit. The immune system appears to play a key role, as the athroprotective effect of estradiol is absent in mice deficient in T and B lymphocytes. Estrogens potentiate the endothelium-dependant relaxation through the increase in nitric oxide bioavailability. Endothelial dysfunction (abnormality of the endothelium-dependent vasodilation) occurs in atheromatous arteries. Estrogens prevent and even correct this endothelial dysfunction. In monkeys, this beneficial effect of estrogens is not altered by coadministration of progesterone, but is abolished.