Abstract
The autonomic nervous system is essential to maintaining tonic and reflex cardiovascular control through the regulation of neural outflow to the heart and circulation. Autonomic modulation of arterial stiffness and hemodynamics can occur reflexively in response to alterations in stroke volume, heart rate, and the mechanical properties of conduit and resistance vessels. Whether acute or chronic increases in sympathetic activity can affect arterial stiffness and pulse wave characteristics independent of changes in distending pressure remains an important physiological question. In this chapter, we discuss the controversies stimulated by human cross-sectional data and recent evidence supporting the concept that acute increases in muscle sympathetic nerve firing can increase central and peripheral arterial stiffness. The moderating effects of neuroendocrine factors on arterial stiffness, including the influence of sex hormones on the relationship between sympathetic outflow and pulse wave characteristics, also will be reviewed.
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