Estrogens and the arterial wall

Two isoforms of oestrogens receptor (alpha and beta) have been identified i n the cells of the arterial wail, and an heterogenity of their expression a ccording to the animal species, to the vascular bed and to sex has been rep orted. Estrogens can thus directly influence the vascular physiology throug h a << genomic >> mechanism, but << extra-genomic >> mechanisms responsible for a short-term effect have also been suggested. Endothelium appears to b e an important target for estradiol, because this hormone potentiates endot helium-dependant relaxation through an increase in NO bioavailability, and accelerates endothelial regrowth. In the model of apolipoprotein E-deficien t mice, as the atrhroprotective effect deposit. The immune system appears t o 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 va sodilation) occurs in atheromatous arteries. Estrogens prevent and even cor rect this endothelial dysfunction. In monkeys, this beneficial effect of es trogens is not altered by coadministration of progesterone, but is abolishe d.