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Because of the high metabolic demands on the heart, oxidative phosphorylation predominates over the less efficient process of anaerobic glycolysis for energy production. Under basal conditions, ∼10% of the body's total oxygen supply is consumed by the heart (O’Rourke et al. 2005). This already staggering requirement rapidly increases during stress. Hence, oxygen bioavailability is a critical determinant of cardiomyocyte function and survival in health and disease. In this issue of The Journal of Physiology, Li et al. (Li et al. 2010) dissect the molecular mechanisms and cell signalling pathways underlying β-adrenergic receptor (AR)-mediated modulation of intracellular oxygen levels during the ‘fight-or-flight’ response. Specifically, these authors demonstrate that β2- and not β1-AR activation acutely increases intracellular oxygen levels through an inhibitory G protein (Gi) pathway, which is dependent on reactive oxygen species (ROS) also generated through this pathway. Indeed, the findings of Li et al. (2010) have far-reaching implications for our understanding of mechanisms underlying a wide variety of stress-related cardiovascular disorders, and can help explain the benefits and pitfalls associated with current therapies for these disorders. |
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