Aortic pressure, substrate utilization and protein synthesis.
An increase in aortic pressure from 60 to 120 mmHg in Langendorff perfused hearts increased oxygen consumption, glucose utilization, pyruvate oxidation and protein synthesis. These changes were not prevented by insertion of a ventricular drain that prevented intraventricular pressure development. Arrest of the heart with tetrodotoxin markedly reduced oxygen consumption; under these conditions an elevation of aortic pressure did not increase oxygen consumption. Elevation of aortic pressure in arrested-drained preparations supplied either glucose or pyruvate as oxidizable substrate increased protein synthesis to a comparable extent. Energy availability, as assessed by measurements of the creatine-P/creatine ratio, increased as aortic pressure was raised in hearts provided glucose, but not pyruvate, suggesting that greater energy availability was not the factor linking higher aortic pressure to faster rates of synthesis. These results focus attention on stretch of the ventricular wall, as the mechanical factor responsible for the effects of aortic pressure on several metabolic activities of the heart.
D000818:Animals; D001011:Aorta / Q000502:physiology*; D001794:Blood Pressure; D006332:Cardiomegaly / Q000209:etiology / Q000378:metabolism; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism*; D006321:Heart; D006324:Heart Arrest, Induced; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D010477:Perfusion; D014176:Protein Biosynthesis; D011773:Pyruvates / Q000378:metabolism*; D019289:Pyruvic Acid; D051381:Rats; D011919:Rats, Inbred Strains; D013314:Stress, Mechanical
D011773:Pyruvates; D019289:Pyruvic Acid; D005947:Glucose