The two isoforms (alpha and beta) of the oestrogen receptor were identified in arterial wall cells. The heterogeneity of their expression is considered according to vascular regions and gender. Oestrogens can have a direct influence on vascular physiology through a "genomic" mechanism of action, although "extragenomic" mechanisms allowing very short-term hormonal action are also possible. Oestrogens potentiate endothelium-dependent relaxation by increasing the bioavailability of nitrogen monoxide (higher production and/or lesser degradation by the superoxide anion as a function of vascular beds). The atheromatous artery is the site of endothelial "dysfunction" (an anomaly of endothelium-dependent vasodilation), which can be prevented and even corrected by administration of oestradiol. In the monkey, this beneficial effect of oestrogens is not altered by addition of progesterone, but abolished by the addition of medroxyprogesterone. Finally, oestrogens prevent formation of the fatty streak. Studies of the mechanism(s) of this effect are now in progress.