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Cardiac alpha 1-adrenergic drive in pathological remodelling Woodcock EA; Du XJ; Reichelt ME; Graham RMCardiovasc Res 2008[Feb]; 77 (3): 452-62The heart is richly innervated by sympathetic nerves, and both acute and chronic regulation of cardiac function via sympathetically released catecholamines acting on cardiomyocyte adrenergic receptors (ARs), is critical for circulatory homeostasis. Cardiomyocytes express alpha 1A- and alpha 1B-, and beta 1- and beta 2-AR subtypes, which are all members of the G-protein-coupled receptor superfamily that signal via interaction with heterotrimeric G-proteins. Cardiac function - both inotropy and chronotropy - is regulated predominantly by beta 1-AR. Activation of alpha 1-ARs also results in increased contractility, as well as changes in the electrophysiological properties and metabolic responses of the heart. Nonetheless, there is little evidence that cardiac alpha 1-ARs play a major functional role under normal physiological conditions. In pathological settings, alpha 1-ARs may function in a compensatory fashion to maintain cardiac inotropy when the beta-AR system is downregulated and uncoupled from G-proteins and effectors. In addition, as we consider here, recent evidence from clinical studies and from genetically engineered animal models indicates that alpha 1-ARs are importantly involved in both developmental cardiomyocyte growth, as well as pathological hypertrophy. In the presence of pressure overload or with myocardial infarction, activation of alpha 1-ARs, particularly the alpha 1A-subtype, also appears to produce important pro-survival effects at the level of the cardiomyocyte, and to protect against maladaptive cardiac remodelling and decompensation to heart failure.|Animals[MESH]|Cardiomegaly/*etiology[MESH]|Genetic Engineering[MESH]|Heart Failure/etiology[MESH]|Humans[MESH]|Hypertension/etiology[MESH]|Myocardial Contraction[MESH]|Myocardial Infarction/etiology[MESH]|Receptors, Adrenergic, alpha-1/*physiology[MESH]|Signal Transduction[MESH]|Ventricular Remodeling[MESH] |
