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Left ventricular (LV) hypertrophy (LVH) is a major determinant of cardiovascular morbidity and mortality; LVH develops in response to valvular disease and hypertension and is part of the remodeling process after myocardial infarction. Initially LVH may serve to reduce wall stress and preserve cardiac output, but more chronically LVH can progress into cardiac decompensation and failure.Transverse aortic constriction is an established animal model to study chronic pressure overload and LVH. In this model, local and/or systemic neurohumoral activation occurs, and circulating norepinephrine and renin concentrations are increased.1 These neurohumoral mediators activate platelets to release ADP and form reactive oxygen species (ROS), endothelial cells to express adhesion molecules and form ROS, fibroblasts to proliferate and synthesize collagen, and cardiomyocytes to synthesize proteins and grow. These divergent effects on different cell types are closely interrelated in that, eg, extracellular ROS contribute to cardiomyocyte hypertrophy and interstitial fibrosis.2Cardiomyocyte growth and adaptive and maladaptive LVH involve activation of phosphoinositide 3-kinase (PI3K; Figure 1). Activation of PI3K-α/β by growth factor receptors and receptor tyrosine kinases is thought to mediate adaptive LVH, whereas PI3K-γ is activated by neurohumoral mediators via G protein–coupled receptors and thought to mediate maladaptive LVH.3 Once activated, PI3Ks generate phosphatidylinositol 3,4,5-triphosphate, leading to the recruitment and activation of Akt/protein kinase B (PKB), which, in turn, activates downstream targets, such as the mammalian …

Extracellular Adenosine Attenuates Left Ventricular Hypertrophy Through Its Impact on the Protein Kinase and Phosphatase Interaction