Floras John S
Sinai Health and University Health Network Division of Cardiology, Toronto General Hospital Research Institute, and the Department of Medicine, University of Toronto.
Hypertension. 2021 May 5;77(5):1456-1468. doi: 10.1161/HYPERTENSIONAHA.121.16490. Epub 2021 Mar 29.
Multiunit recordings of postganglionic sympathetic outflow to muscle yield otherwise imperceptible insights into sympathetic neural modulation of human vascular resistance and blood pressure. This Corcoran Lecture will illustrate the utility of microneurography to investigate neurogenic cardiovascular regulation; review data concerning muscle sympathetic nerve activity of women and men with normal and high blood pressure; explore 2 concepts, central upregulation of muscle sympathetic outflow and cortical autonomic neuroplasticity; present sleep apnea as an imperfect model of neurogenic hypertension; and expose the paradox of sympathetic excitation without hypertension. In awake healthy normotensive individuals, resting muscle sympathetic nerve activity increases with age, sleep fragmentation, and obstructive apnea. Its magnitude is not signaled by heart rate. Age-related changes are nonlinear and differ by sex. In men, sympathetic nerve activity increases with age but without relation to their blood pressure, whereas in women, both rise concordantly after age 40. Mean values for muscle sympathetic nerve activity burst incidence are consistently higher in cohorts with hypertension than in matched normotensives, yet women's sympathetic nerve traffic can increase 3-fold between ages 30 and 70 without causing hypertension. Thus, increased sympathetic nerve activity may be necessary but is insufficient for primary hypertension. Moreover, its inhibition does not consistently decrease blood pressure. Despite a half-century of microneurographic research, large gaps remain in our understanding of the content of the sympathetic broadcast from brain to blood vessel and its specific individual consequences for circulatory regulation and cardiovascular, renal, and metabolic risk.
对节后交感神经向肌肉的传出进行多单位记录，能让人洞察交感神经对人体血管阻力和血压的调节，而这些洞察在其他情况下是难以察觉的。本次科克伦讲座将阐述微神经ography在研究神经源性心血管调节方面的实用性；回顾有关血压正常和高血压的男性及女性肌肉交感神经活动的数据；探讨两个概念，即肌肉交感神经传出的中枢上调和皮质自主神经可塑性；将睡眠呼吸暂停作为神经源性高血压的一个不完美模型进行探讨；并揭示交感神经兴奋但无高血压这一矛盾现象。在清醒的健康血压正常个体中，静息肌肉交感神经活动会随着年龄增长、睡眠片段化和阻塞性呼吸暂停而增加。其幅度与心率无关。与年龄相关的变化是非线性的，且存在性别差异。在男性中，交感神经活动随年龄增长而增加，但与血压无关，而在女性中，40岁以后两者会同步上升。高血压人群中肌肉交感神经活动爆发发生率的平均值始终高于匹配的血压正常者，然而女性的交感神经流量在30岁至70岁之间可增加3倍而不引发高血压。因此，交感神经活动增加可能是原发性高血压的必要条件，但并不充分。此外，对其抑制并不一定会持续降低血压。尽管进行了半个世纪的微神经ography研究，但在我们对从大脑到血管的交感神经信号内容及其对循环调节以及心血管、肾脏和代谢风险的具体个体影响的理解方面，仍存在巨大差距。
