Different mechanisms in the hepatic actions of estrogens

Literary data proved evidence that uterine actions of estrogens develop through different receptor systems. We performed experiments to examine whether different mechanisms are also involved in the hepatic effects of estrogenic steroids. Female rats were treated with a single dose of 5 mg/kg estrone. Dry liver weight and protein content increased. Both responses were blocked by prior administration of natural antiestrogen progesterone. Increased wet organ weight and water content were measured as edematous reactions. They can be attributed to the depolymerisation of mucopolysaccharides. Progesterone could not prevent these effects. Estrone induced glycogen synthesis in the liver. This was counteracted by progesterone treatment. To elucidate the possible role of the adenylcyclase system the animals were treated with beta-receptor blocker propranolol which had no effect either on liver glycogen content or on estrone induced synthesis. Dihydroergocryptine, an equal blocker of alpha 1- and alpha 2-receptors, did not interfere with glycogenetic action of estrone either. The selective alpha 1-receptor blocker prazosin decreased the liver glycogen content and inhibited glycogenetic response to estrone. Our results proved that estrogens display their hepatic effects by several mechanisms that can be selectively blocked or moderated.