From Brain to Blood Vessel: Insights From Muscle Sympathetic Nerve Recordings

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.