Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia.
Exp Physiol. 2011 Jul;96(7):611-22. doi: 10.1113/expphysiol.2010.052332. Epub 2011 May 6.
The 17th century London neuroanatomical school headed by Thomas Willis provided us with the first identifiable images of the sympathetic nervous system. Nineteenth century giants of European physiology (Bernard, Waller and Brown-Sequard) identified these as the 'pressor nerves'. Von Euler's demonstration that the sympathetic transmitter was noradrenaline brought the field into the modern era. The development of ganglion-blocking drugs by Paton, whose name this review commemorates, allowed comprehensive pharmacological antagonism of this system in patients. With the development of contemporary techniques for recording from human sympathetic nerves and quantifying rates of noradrenaline release, the sympathetic nervous system became accessible to clinical scientists investigating possible contributions to cardiovascular and other diseases. Sympathetic nervous system responses typically are regionally differentiated, with activation in one outflow sometimes accompanying no change or sympathetic inhibition in another. Regional sympathetic activity is best studied in humans by recording from postganglionic sympathetic efferents (multi-unit or single-fibre recording) and by isotope dilution-derived measurement of organ-specific noradrenaline release to plasma from sympathetic nerves (regional 'noradrenaline spillover'). With the application of these techniques, evidence has been assembled in the past three decades which indicates that sympathetic nervous system activation is crucial in the development of cardiovascular disorders, most notably heart failure and essential hypertension. An important goal for clinical scientists is translation of knowledge of pathophysiology, such as this, into better treatment for patients. The achievement of this 'mechanisms to management' transition is mature in cardiac failure, with knowledge of cardiac neural pathophysiology having led to introduction of β-adrenergic blockers, an effective therapy. Perhaps we are now on the cusp of effective translation in patients with essential hypertension, with recent successful testing of selective catheter-based renal sympathetic nerve ablation in patients with resistant hypertension, an intervention firmly based on prior demonstration in them of activation of the renal sympathetic outflow.
17 世纪由托马斯·威利斯（Thomas Willis）领导的伦敦神经解剖学派为我们提供了最早可识别的交感神经系统图像。19 世纪欧洲生理学的巨头（伯纳德、沃勒和布朗-塞夸德）将其鉴定为“升压神经”。冯·埃勒（von Euler）证明交感神经递质是去甲肾上腺素，使该领域进入了现代时代。帕顿（Paton）开发的神经节阻滞药物，其名字是本综述纪念的对象，使该系统在患者中得到了全面的药理学拮抗。随着用于从人类交感神经记录和量化去甲肾上腺素释放率的当代技术的发展，交感神经系统开始为研究可能对心血管和其他疾病有贡献的临床科学家所研究。交感神经反应通常具有区域性差异，一种传出神经的激活有时伴随着另一种传出神经没有变化或抑制。通过记录节后交感传出神经（多单位或单纤维记录）和通过从交感神经测量器官特异性去甲肾上腺素释放到血浆的同位素稀释法（区域性“去甲肾上腺素溢出”），可以最好地在人体中研究局部交感活性。应用这些技术，在过去三十年中已经积累了证据，表明交感神经系统的激活在心血管疾病的发展中至关重要，尤其是心力衰竭和原发性高血压。临床科学家的一个重要目标是将生理学知识，例如这种知识，转化为对患者更好的治疗。从心脏神经生理学知识中获得的心力衰竭知识已经导致β-肾上腺素能阻滞剂的引入，这是一种有效的治疗方法，这种“从机制到管理”的转变已经在心力衰竭中成熟。也许我们现在正处于原发性高血压患者有效转化的边缘，最近对有抵抗性高血压的患者进行选择性导管肾交感神经消融术的成功测试，这种干预措施基于对肾交感传出神经激活的先前证明。
