Sympathetic neural mechanisms in human cardiovascular health and disease

Abstract

The sympathetic nervous system plays a key role in regulating arterial blood pressure in humans. This review provides an overview of sympathetic neural control of the circulation and discusses the changes that occur in various disease states, including hypertension, heart failure, and obstructive sleep apnea. It focuses on measurements of sympathetic neural activity (SNA) obtained by microneurography, a technique that allows direct assessment of the electrical activity of sympathetic nerves in conscious human beings. Sympathetic neural activity is tightly linked to blood pressure via the baroreflex for each individual person. However, SNA can vary greatly among individuals and that variability is not related to resting blood pressure; that is, the blood pressure of a person with high SNA can be similar to that of a person with much lower SNA. In healthy normotensive persons, this finding appears to be related to a set of factors that balance the variability in SNA, including cardiac output and vascular adrenergic responsiveness. Measurements of SNA are very reproducible in a given person over a period of several months to a few years, but SNA increases progressively with healthy aging. Cardiovascular disease can be associated with substantial increases in SNA, as seen for example in patients with hypertension, obstructive sleep apnea, or heart failure. Obesity is also associated with an increase in SNA, but the increase in SNA among patients with obstructive sleep apnea appears to be independent of obesity per se. For several disease states, successful treatment is associated with both a decrease in sympathoexcitation and an improvement in prognosis. This finding points to an important link between altered sympathetic neural mechanisms and the fundamental processes of cardiovascular disease.

FIGURE 1.

Electrocardiogram (ECG), integrated sympathetic neurogram, and plot of beat-to-beat arterial pressure (AP) (as measured by a brachial artery catheter) from a healthy person. The figure shows the dynamic relationship between AP and muscle sympathetic neural activity (MSNA). The shading highlights an example of a transient decrease in AP that elicits an increase in MSNA via the baroreflex. This increase causes vasoconstriction, which in turn increases AP and leads to a reflex decrease in MSNA.

FIGURE 2.

Electrocardiogram (ECG), integrated sympathetic neurogram, and plot of beat-to-beat arterial pressure (AP) from a healthy person. The ECG tracing shows a premature ventricular contraction that is associated with an ineffective beat. The subsequent decrease in diastolic pressure elicits a large reflex burst of muscle sympathetic neural activity (MSNA). The arrow indicates the relationship between the low diastolic pressure and the elicited burst of MSNA.

FIGURE 3.

Resting values for muscle sympathetic neural activity (MSNA) and mean arterial pressure in 41 healthy men. The figure shows the absence of an association between these variables. Although MSNA values range widely among healthy persons, the arterial pressure levels are not consistently higher among persons with very high MSNA than among those with much lower MSNA.