Some metabolic features of the development of experimentally induced cardiac hypertrophy.

Abstract

The possible mechanisms responsible for the enhancement of adenine nucleotide and protein synthesis in rat hearts developing experimentally induced hypertrophy were examined. To assess the involvement of catecholamines, two approaches were used. (1) The content of myocardial cyclic AMP (cAMP) was determined and correlated with the changes in protein synthesis. In cardiac hypertrophy induced by isproterenol and truodothyronine, the cAMP level was elevated, and this elevation preceded the enhancement of protein synthesis. In hypertrophy due to aortic constriction, however, the increase in cardiac cAMP was only moderate and did not occur prior to but concomitant with the enhancement of protein synthesis. (2) β-Receptor blockade with propranolol was performed in all three types of hypertrophy studied was well as in rats with myocardial infarction produced by ligation of the descending branch of the left coronary artery. The stimulation of cardiac adenine nucleotide biosynthesis in isoproterenol and truodothyronine-elicited hypertrophy was prevented by propranolol. However, propranolol did not affect the enhancement of adenine nucleotide and protein synthesis in the pressure-overloaded heart and in the non-infarcted myocardium. These results may be taken to indicate that different mechanisms are involved in the stimulation of adenine nucleotide and protein synthesis in various models of cardiac hypertrophy.