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lüll Na/K-ATPase--an integral player in the adrenergic fight-or-flight response Bers DM; Despa STrends Cardiovasc Med 2009[May]; 19 (4): 111-8During activation of the sympathetic nervous system, cardiac performance is increased as part of the fight-or-flight stress response. The increase in contractility with sympathetic stimulation is an orchestrated combination of intrinsic inotropic, lusitropic, and chronotropic effects, mediated in part by activation of beta-adrenergic receptors and protein kinase A. This causes phosphorylation of several Ca cycling proteins in cardiac myocytes (increasing Ca entry via L-type Ca channels, sarcoplasmic reticulum Ca pumping, and the dissociation rate of Ca from the myofilaments). Here, we discuss how stimulation of the Na/K-ATPase, mediated by phosphorylation of phospholemman (a small sarcolemmal protein that associates with and modulates Na/K-ATPase), is an additional important player in the sympathetic fight-or-flight response. Enhancement of Na/K- ATPase activity limits the rise in [Na](i) caused by the higher level of Na influx and by doing so limits the rise in cellular and sarcoplasmic reticulum Ca load by favoring Ca extrusion via the Na/Ca exchanger. Thus, phospholemman-mediated activation of the Na/K-ATPase may prevent Ca overload and triggered arrhythmias during stress.|*Escape Reaction[MESH]|*Myocardial Contraction[MESH]|Arrhythmias, Cardiac/metabolism/physiopathology/prevention & control[MESH]|Calcium Signaling[MESH]|Cyclic AMP-Dependent Protein Kinases/metabolism[MESH]|Heart Rate[MESH]|Heart/*innervation[MESH]|Humans[MESH]|Membrane Proteins/metabolism[MESH]|Myocardium/*enzymology[MESH]|Phosphoproteins/metabolism[MESH]|Phosphorylation[MESH]|Receptors, Adrenergic, beta/metabolism[MESH]|Sodium-Calcium Exchanger/metabolism[MESH]|Sodium-Potassium-Exchanging ATPase/*metabolism[MESH]|Sodium/metabolism[MESH]|Sympathetic Nervous System/*metabolism[MESH] |