Abstract
The increase in myocardial contractile force after administration of epinephrine is closely related to the activation of cyclic 3', 5'-AMP with a subsequent conversion of phosphorylase b to a (1-5). Further, it seems likely that there exists a close relationship between the level of circulating catecholamine and the activity of phosphorylase in the heart, based on the finding that the injection of ganglionic stimulating agents produces the simultaneous increase in myocardial contractile force and augmentation of phosphorylase activity (6). The observation of Nakatani (7) that physostigmine augments phosphorylase activity in the heart and this augmentation is prevented by prior reserpine is compatible with the view that endogenously liberated catecholamines increase phosphorylase a.
However, there are controversial reports regarding the effect of reserpine on heart phosphorylase activity: no significant change (3, 8), increase (5) and decrease (9), and there is no conclusive evidence that reserpine decreases heart phosphorylase. This is incompatible with the concept that there is a positive correlation between the amount of endogenous catecholamines and heart phosphorylase a activity. All these expriments, however, were conducted in the in situ preparations. To our knowledge, the one exceptional observation was made by Giotti (10), who reported insignificant effects of reserpine in vitro on phosphorylase activity in guinea pig atria.
The present study was undertaken to investigate the relationship between reserpine and phosphorylase activity in the isolated rabbit atria.
