Mitochondrial respiratory control in the myocardium.
The heart muscle has proved to be a practical model for studying respiratory control in intact tissues. It also demonstrates that control at the level of the respiratory chain is augmented by metabolic control at the substrate level as exemplified by the very narrow range of changes in the redox state of the mitochondrial NADH/NAD couple even during extensive changes in ATP and oxygen consumption. The behaviour of mitochondria when isolated can largely be duplicated in the intact myocardium. Moreover, the high intracellular concentrations of enzymes, coenzymes and adenine nucleotides create conditions of high reaction rates, enabling the formation of a near equilibrium network of certain main pathways. This equilibrium network in connection with metabolic regulation of the hydrogen pressure upon the matrix NADH/NAD pool is a prerequisite for the regulation of cellular respiration at a high efficiency of energy transfer. Experimentation on the intact myocardium also seems to be capable of resolving some of the uncertainties about prevailing mechanisms for the regulation of cellular respiration.
D000244:Adenosine Diphosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003402:Creatine Kinase / Q000378:metabolism; D004563:Electrochemistry; D004734:Energy Metabolism; D006859:Hydrogen / Q000378:metabolism; D066298:In Vitro Techniques; D008929:Mitochondria, Heart / Q000201:enzymology / Q000378:metabolism*; D008954:Models, Biological; D009206:Myocardium / Q000166:cytology / Q000378:metabolism; D010084:Oxidation-Reduction; D010101:Oxygen Consumption
D000244:Adenosine Diphosphate; D006859:Hydrogen; D000255:Adenosine Triphosphate; D003402:Creatine Kinase