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Abstract
Background: Norepinephrine (NE) is released from its storage granules when the nerve is stimulated and enters the synaptic cleft to bind to alpha and beta-receptors on the effector cells. Chemical signaling is terminated by a rapid reuptake of neurotransmitter into presynaptic nerve terminals mainly via NE transport systems (NET). Previous studies in animal model of heart failure showed that both increased neuronal release of NE and decreased efficiency of NET contribute to decreased myocardial NE content which correlates directly with decreasing the left ventricular ejection fraction.
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