Neural influences on cardiovascular variability: possibilities and pitfalls.

Abstract

Altered variability in the cardiovascular system is associated with a range of cardiovascular diseases and increased mortality. Because blood pressure and heart rate show distinct low-frequency oscillations that appear to be affected by either vagal or sympathetic activity, it has been hoped that measurement of the strength of these oscillations could be used as an index of autonomic tone and thus form the basis of a diagnostic test. This review focuses on recent research that has examined the fundamental origin of variability associated with respiration and a slow oscillation at 0.1 Hz in the human. A new hypothesis is proposed to account for the slow oscillation in heart rate and blood pressure that incorporates components of the central nervous system, other reflex pathways regulating sympathetic activity, and resonance in the baroreflex control of blood pressure. Whereas it is clear that sympathetic activity and arterial baroreflexes are critical elements in producing cardiovascular variability, there is also evidence that other factors, including the ability of the vasculature to respond to sympathetic activity, appear to play a role in determining the strength of oscillations. Given the potential impact of other nonbaroreflex or nonautonomic pathways in affecting cardiovascular variability, it is proposed that one must use care in relating changes in the strength of an oscillation in blood pressure and heart rate as definitively due to a change in autonomic control.