Integration of glucose transport with metabolic and functional activity of heart muscle.
The role of glucose transport modulation in adjusting myocardial energy supply to changing contractile and metabolic activity and to hormonal influences was studied. Because membrane transport is a rate-limiting step in glucose utilization, many physiological and pharmacological influences act at this step. These include muscular contraction, insulin, adrenaline, inotropic interventions. Na+ pump activity alterations, some heavy metal ions, and other Ca2+ antagonists. All these agents affect the sarcolemmal fluxes and/or the intracellular distribution of Ca2+, and the evidence is consistent with their effects on sugar transport being linked to their ability to alter the availability of cytoplasmic Ca2+. This is the basis for the hypothesis that sugar transport in muscle is regulated by Ca2+ binding to specific regulatory sites. Two positive controls, through contraction and insulin, and two negative feedbacks from mitochondrial oxidation and activity of the Na+ pump are identified.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D004837:Epinephrine / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism*; D006168:Guinea Pigs; D006339:Heart Rate; D066298:In Vitro Techniques; D007328:Insulin / Q000494:pharmacology; D008660:Metabolism / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism*; D010042:Ouabain / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000378:metabolism
D007328:Insulin; D010042:Ouabain; D012964:Sodium; D005947:Glucose; D002118:Calcium; D004837:Epinephrine