Different mechanisms in the hepatic actions of XXXX .

@entity172 @entity1169 @entity1420 @entity35 @entity4 @entity3159 @entity1815 @entity230 @entity71037
Literary data proved evidence that uterine actions of @entity172 develop through different receptor systems. We performed experiments to examine whether different mechanisms are also involved in the hepatic effects of estrogenic @entity230 . Female @entity35 were treated with a single dose of 5 mg/kg @entity1815 . Dry liver weight and protein content increased. Both responses were blocked by prior administration of natural antiestrogen @entity1420 . Increased wet organ weight and water content were measured as @entity4 . They can be attributed to the depolymerisation of mucopolysaccharides. @entity1420 could not prevent these effects. @entity1815 induced glycogen synthesis in the liver. This was counteracted by @entity1420 treatment. To elucidate the possible role of the adenylcyclase system the animals were treated with beta-receptor blocker @entity1169 which had no effect either on liver glycogen content or on @entity1815 induced synthesis. @entity71037 , an equal blocker of alpha 1- and alpha 2-receptors, did not interfere with glycogenetic action of @entity1815 either. The selective alpha 1-receptor blocker @entity3159 decreased the liver glycogen content and inhibited glycogenetic response to @entity1815 . Our results proved that @entity172 display their hepatic effects by several mechanisms that can be selectively blocked or moderated.
