Autoregulation of myocardial glycogen concentration during intermittent hypoxia
Autor: | P. H. McNulty, C. Ng, D. Jagasia, J. C. Baldwin, R. Soufer, G. V. Letsou, Wenli Liu |
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Rok vydání: | 1996 |
Předmět: |
Male
medicine.medical_specialty Glycogenolysis Physiology Glucose-6-Phosphate Blood Pressure Glycogen debranching enzyme Rats Sprague-Dawley chemistry.chemical_compound Heart Rate Physiology (medical) Internal medicine medicine Glycogen branching enzyme Animals Homeostasis Insulin Glycogen synthase Hypoxia biology Glycogen Myocardium Osmolar Concentration Intermittent hypoxia Hypoxia (medical) Myocardial Contraction Propranolol Rats Oxygen Endocrinology Glycogen Synthase chemistry Glycogenesis biology.protein Heart Transplantation Gases medicine.symptom |
Zdroj: | The American journal of physiology. 271(2 Pt 2) |
ISSN: | 0002-9513 |
Popis: | During hypoxia, the heart consumes glycogen to generate ATP. Tolerance of repetitive hypoxia logically requires prompt replenishment of glycogen, a process whose regulation is not fully understood. To examine this, we imposed a defined hypoxic stimulus on the rat heart while varying its workload. In intact rats, hypoxia reduced myocardial glycogen approximately 30% and increased both the fraction of glycogen synthase in its physiologically active (GS I) form (from 0.24 +/- 0.06 to 0.82 +/- 0.07; P < 0.005) and glycogen synthesis (from 0.087 +/- 0.011 to 0.375 +/- 0.046 mumol.g-1.min-1; P < 0.005). Reducing cardiac work (with propranolol or heterotopic transplantation) reduced glycogen breakdown, glycogen synthase activation, and glycogen synthesis in parallel, stepwise fashion in intact rats. Correspondingly, hypoxia increased GS I activity in the perfused heart in vitro, but only under conditions where glycogen was consumed. This suggests myocardial glycogen synthase is activated by systemic hypoxia and catalyzes rapid posthypoxic glycogen synthesis. Hypoxic glycogen synthase activation appears to be a proportionate, wholly intrinsic response to local glycogenolysis, operating to preserve myocardial glycogen stores independent of any extracardiac mediator of carbohydrate metabolism. |
Databáze: | OpenAIRE |
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