Metabolic aspects of the development of experimental cardiac hypertrophy.
In three models of cardiac hypertrophy the significance of catecholamines and the adenylate cyclase-cyclic AMP-system was examined. Two approaches were utilized: 1. The time course of cyclic AMP alterations was correlated with the changes in adenine nucleotide and protein biosynthesis. 2. The effect of beta-receptor blockade on the obligatory increase in adenine nucleotide and protein synthesis was evaluated. In isoproterenol-elicited cardiac hypertrophy, the elevation of the cyclic AMP content was one of the earliest metabolic alterations preceding the enhancement of the biosynthesis of adenine nucleotides and proteins. beta-Receptor blockade with propranolol abolished the increase in adenine nucleotide synthesis. In pressure-induced cardiac hypertrophy due to constriction of the abdominal aorta, catecholamines and the adenylate cyclase-cyclic AMP-system were found not to play a significant role. In triiodothyronine-elicited hypertrophy, the cyclic AMP level was increased very early, but beta-receptor blockade did not prevent hypertrophy nor the enhancement of cardiac adenine nucleotide biosynthesis, although the positive chronotropic and inotropic effects of triiodothyronine were abolished. This result can best be interpreted to indicate a direct effect of triiodothyronine on myocardial carbohydrate metabolism including the pentose phosphate pathway.
D000227:Adenine Nucleotides / Q000096:biosynthesis / Q000378:metabolism*; D000818:Animals; D006332:Cardiomegaly / Q000209:etiology / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D009124:Muscle Proteins / Q000096:biosynthesis*; D009206:Myocardium / Q000378:metabolism*; D051381:Rats
D000227:Adenine Nucleotides; D009124:Muscle Proteins; D000242:Cyclic AMP