Studies on adenyl cyclase system in myocardium (Part I). Adenyl cyclase system in the hypertrophied and failing rabbit hearts.

Many reports state a marked reduction of catecholamine (CA) in cardiac tissue and an increased CA concentration of serum and urine in patients with congestive heart failure 1)-5). Thus, it is assumed that the function of the impared heart might be supported by the increased blood CA. It has been reported that the inotropic 6)-12) and chronotropic response 13)-16) of CA to the cardiovascular system are mediated by adenyl cyclase-cyclic AMP system. Adenyl cyclase-cyclic AMP system was initially discovered as the intracellular mediator of the glycogenolytic effects of epinephrine and glucagon in the liver by Sutherland and Rall l ?), but it has since come to be recognized as a second messenger mediating a variety of hormonal effects I8)-20). It is proposed that CA activates adenyl cyclase and increases intracellular cyclic AMP by converting ATP to cyclic AMP which mediates inotropic action as a 2nd messenger. Furthermore, the concentration of intracellular cyclic AMP is controlled both by adenyl cyclase, the synthesizing enzyme, and phosphodiesterase, the. converting enzyme. In order to investigate CA and adenyl cyclase-cyclic AMP system in cardiac failure" the changes of myocardial CA concentration, adenyl cyclase and phosphodiesterase activity in the hypertrophied and failing heart were investigated using experimental aortic stenosis of rabbits.