The Effect of Physostigmine on Heart Phosphorylase Activity in the Spinal Rat.

中谷 〓二 It was reported previously (1) that an increase in heart phosphorylase a following the intravenous administration of adrenaline in a dose of 10.0 ƒÊg/kg was less than that following 1.0 ƒÊg/kg, and that atropinization or vagotomy potentiated the phosphorylase activating action of adrenaline. In addition, a significant elevation of heart phospho rylase a was maintained for 2 hours after the injection of 1.0 ƒÊg/kg of adrenaline. From the results, it was suggested that the reflectively released endogenous acetylcholine inhibited the phosphorylase-activating action of adrenaline, and that the long-lasting elevation of heart phosphorylase a even after disappearance of the positive inotropic action of adrenaline was related to the uptake or storage mechanism of adrenaline in the heart tissue. Many investigators (2-6) demonstrated that the positive inoand chrono-tropic responses to exogenous adrenaline of the heart were closely related to the activation of formation of cyclic 3',5'-AMP with subsequent conversion of phosphorylase b to a. The finding (7) that injection of ganglionic stimulating agents such as DMPP and McNeil A-343 produced an increase in heart phosphorylase a with concomitant hypertension and increase in cardiac contractile force may suggest a relationship between the level of circulating catecholamine endogenously liberated and the activity of phosphorylase in the heart. However, there are controversial reports regarding the effect of reserpine on heart phosphorylase activity : no significant change (4, 8), increase (6), and decrease