High doses of propranolol give rise to a liver disenzymic injury by depression of its clearance and colloidopexic functions, but without any histological change. The molecular target responsible for this disturbance seems to lie at the level of ATP-ase, because propranolol stimulates the membrane activity and supresses the citochondrial one. There are described some effects of this drug and its pharmocological opposite, isopropylenorepinephrine, on the liver cell enzymes, which may serve as a morphological proof of the antagonism between the mitochondrial and plasmalemal ATP-ase activity, on the one hand, and of the membrane ATP-ase and AMP-cyclase, on the other hand.