This study was designed to elucidate the effects of iron, a well known catalyst of lipid peroxidation, on the contents of phospholipids, unsaturated fatty acids composed in phospholipid molecules and their derivatives, prostaglandins, and the composition changes of fatty acids contained in phospholipids. Iron decreased the contents of phospholipids and its components of unsaturated fatty acids. Catalytic action of iron decreased the composition rates of linoleate and linolenate composed in phospholipid molecules, while that of arachidonate was inclined to increase. The content of arachidonate was increased and that of prostaglandins was decreased without regard to increase the precursor of prostaglandins. It may be concluded that the decreases of the activities of prostaglandins and the increase of arachidonate are due to inhibition of the activities of enzyme systems responsible for prostaglandin synthesis by lipid peroxides produced by the catalyst of iron

To examine the selectivity of verapamil, used in the cardiovascular diseases, on alpha-1 and alpha-2 adrenoceptor-induced pressor responses, effects of verapamil on alpha-adrenoceptor agonist-induced pressor responses were investigated in urethane-anesthetized rabbits, spinal rabbits, rats and pithed rats. To evaluate the effects of verapamil on each pressor response induced by norepinephrine, phenylephrine and clonidine, these agonists were previously injected into an ear vein, and the same procedures were performed 1-2 min after treatment with intravenous verapamil. Intravenous verapamil produced dose-dependent depressor response in rabbits and rats. Pressor responses to intravenous norepinephrine (10 micro g/kg) and phenylphrine (30 micro g/kg) were inhibited by pretreatment with intravenous verapamil in rabbits and no difference was noted between the degree of both inhibitions of the pressor response by verapamil. Pressor responses to intravenous norepinephrine (3 micro g/kg), phenylephrine (20 micro/kg) and clonidine (300 micro g/kg) were inhibited by pretreatment with intravenous verapamil in spinal rabbits. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by verapamil. The inhibition of clonidine-induced pressor response by verapamil was more prominent than that of norepinephrine- or phenylephrine-induced pressor response. Pressor responses to intravenous norepinephrine (3 micro g/kg) and phenylephrine (10 micro g/kg) were inhibited by pretreatment with intravenous verapamil in rats and no difference was noted between the degree of both inhibitions of the pressor response by verapamil