Sympathetic Signatures of Cardiovascular Disease

摘要

See related article, pp 634–641Sympathetic nervous system activity is increased in several cardiovascular diseases, including hypertension and heart failure (HF).1 Indeed, one classification of the severity of HF is based on the direct relationship between the plasma concentration of the sympathetic neurotransmitter, norepinephrine, and impaired cardiac function.1 Although the role of increased sympathetic nerve activity (SNA) in the pathogenesis of cardiovascular disease is still debated, it is now accepted that many of the pathologies common to several of these diseases, such as endothelial dysfunction, vascular and cardiac remodeling, and dysregulation of glucose metabolism, are linked to excessive activity of the sympathetic nervous system.1Pharmacological treatments for the deleterious effects of increased sympathetic nervous system activity have been in use for >50 years. These strategies have progressed from sympatholytic drugs used in the 1950s (eg, reserpine), which act peripherally to prevent the synthesis and release of norepinephrine from sympathetic nerve terminals, to α- and β-adrenergic receptor antagonists (eg, prazosin and atenolol, respectively), to centrally acting drugs (eg, clonidine), which reduce sympathetic nerve discharge by their actions in the brain.2 Although these drugs are effective to varying degrees in the treatment of cardiovascular diseases, such as hypertension and HF, they all act in a “global” manner and, therefore, are associated with unwanted adverse effects related to their cardiovascular and noncardiovascular actions.Over the last 20 years it has become clear that the idea that sympathetic activity is either increased or decreased in various physiological and pathophysiological states is an oversimplification. Rather, the pattern of SNA to individual targets, such as the heart, kidneys, splanchnic organs, and skeletal …