Mechanisms of synthesis of purine nucleotides in heart muscle extracts.

The key role of ATP, a purine nucleotide, in the conversion of chemical energy into mechanical work by myocardial tissue is well established (1, 2). The requirement for purine nucleotides has also been demonstrated in the multiple synthetic reactions which maintain all animal cells in the steady state. Since the question immediately arises whether the purine nucleotides are themselves in a steady state, in which their rates of synthesis equal their rates of degradation, it seems reasonable to investigate first what mechanisms of synthesis and degradation may be operative. At present, there are three known pathways for the synthesis of purine nucleotides. The first is the synthesis de novo of the purine ring from small molecular weight precursors, such as glycine, formate, CO2, glutamine and aspartic acid (3). The initial steps in this synthesis (4, 5) are as follows: