[Effects of estrogens on the vascular wall: cellular and molecular mechanisms].
There is evidence from animal models and in vitro experiments that estrogens exert direct effects on the vascular wall. 17 beta-estradiol mediates vasodilatation and inhibits smooth muscle cell proliferation/migration. Furthermore, it modulates the vascular inflammatory response by inhibiting cytokine activation and expression of cell adhesion molecules. Finally, 17 beta-estradiol inhibits platelet aggregation and adhesion. Thus, vasoprotection by estrogens is mediated via genomic and nongenomic pathways. Estrogens regulate gene expression by interacting with estrogen receptors (ER) and other transcription factors. The possible estrogen actions include nongenomic stimulation of membrane mediators and second messenger systems. The existence of two ER subtypes alpha and beta indicates the potential of different biological estrogen effects. At present, the expression, the relation, and the biological actions of ER alpha and beta in different vascular beds of origin, in female and male as well as in healthy and atherosclerotic blood vessels are not known.
Joswig
M
M
Innere Medizin I, Endokrinologie und Stoffwechsel, Universität Heidelberg.
D001161:Arteriosclerosis / Q000503:physiopathology; D004958:Estradiol / Q000494:pharmacology*; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D005260:Female; D006801:Humans; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D010973:Platelet Adhesiveness / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D011960:Receptors, Estrogen / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects
D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D010975:Platelet Aggregation Inhibitors; D011960:Receptors, Estrogen; D004958:Estradiol