Function of the Sympathetic Nervous System
The sympathetic nervous system prepares the body for "fight or flight" responses by increasing heart rate, enhancing cardiac contractility, constricting blood vessels, releasing catecholamines from the adrenal medulla, and mobilizing energy stores to meet acute physiological demands. 1, 2
Primary Cardiovascular Effects
The sympathetic nervous system exerts its cardiovascular effects through multiple mechanisms:
Cardiac stimulation: Sympathetic activation increases heart rate (positive chronotropic effect), enhances myocardial contractility (positive inotropic effect), and improves conduction velocity through the heart 3, 1
Vascular regulation: Activation of alpha-1 adrenergic receptors on vascular smooth muscle causes vasoconstriction and increases peripheral resistance, while beta-2 receptors in coronary arteries produce vasodilation to meet increased myocardial oxygen demand during sympathetic activation 3, 1
Catecholamine release: Sympathetic stimulation triggers release of norepinephrine from nerve terminals and epinephrine from the adrenal medulla, which act on alpha and beta adrenergic receptors throughout the body 1, 2
Anatomical Organization
The sympathetic outflow originates from specific regions of the central nervous system:
Spinal origin: Preganglionic sympathetic neurons arise from the intermediolateral cell column of the thoracolumbar spinal cord (T1-L2), with cardiac sympathetic fibers typically originating from T1-T5 or T6 segments 3, 4
Central control: Command neurons in the hypothalamus and brainstem provide coordinated input to sympathetic preganglionic neurons, enabling parallel activation of multiple sympathetic pathways during stress responses 2
Peripheral ganglia: Preganglionic fibers synapse with postganglionic neurons in paravertebral ganglia or prevertebral ganglia (via splanchnic nerves), which then innervate target organs 3, 4
Physiological Regulation and Modulation
The sympathetic nervous system demonstrates sophisticated regulatory patterns:
Heart rate variability effects: Sympathetic activation acts as a low-pass filter on heart rate variability, allowing primarily low-frequency fluctuations (around 0.1 Hz) while suppressing higher frequency variations, and paradoxically reduces overall heart rate variability despite increasing the relative proportion of low-frequency components 5, 4
Blood pressure regulation: Sympathetic outflow plays a crucial role in both short-term and long-term blood pressure control, with individual variability in sympathetic tone contributing to differences in baseline blood pressure and hypertension risk 6, 7
Homeostatic functions: Beyond acute stress responses, the sympathetic nervous system maintains homeostasis during daily activities including exercise, eating, and thermoregulation 8
Clinical Implications
Understanding sympathetic function is essential for managing cardiovascular disease:
Beta-blocker therapy: These medications reduce heart rate and contractility by blocking sympathetic effects at cardiac beta-1 receptors, effectively antagonizing sympathetic drive—a cornerstone of heart failure management per the American College of Cardiology 5, 9
Pathological activation: Chronic sympathetic overactivity contributes to adverse cardiovascular remodeling, including ventricular hypertrophy, myocardial ischemia, arrhythmias, and apoptosis through sustained norepinephrine exposure 5
Arrhythmia triggers: Sympathetic stimulation can provoke atrial fibrillation during exercise in susceptible individuals, while autonomic imbalance more broadly contributes to various arrhythmic disorders 4
Common Pitfalls
Misinterpreting heart rate variability: The absolute power in the low-frequency band does NOT reflect sympathetic activity; only the relative proportion of low-to-high frequency power provides an approximate indication of sympathetic modulation 5, 4
Assuming class effects: Not all beta-blockers provide equivalent cardiovascular benefits—only bisoprolol, sustained-release metoprolol succinate, and carvedilol have proven mortality reduction in heart failure trials 5
Overlooking metabolic effects: Beta-3 adrenergic receptors in adipose tissue increase fat oxidation and energy expenditure, representing an important metabolic dimension of sympathetic function 1