Involvement of the sympathetic nervous system in congestive heart failure is characterized by a vicious circle, where reduced cardiac output results in neurohumoral activation. The hyperadrenergic state in turn causes desensitization and downregulation of cardiac β-adrenergic receptors and alterations of postsynaptic signal transduction, which further impair myocardial performance. Alterations of presynaptic cardiac sympathetic innervation are also involved in this pathophysiologic process. Reduction of presynaptic catecholamine reuptake increases overexposure to catecholamines further and thereby contributes to disease progression.
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