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The cardiac sympathetic nervous system (CSNS) is an anatomical and physiological network that provides extrinsic regulation of cardiac function. It originates from the preganglionic neurons in the thoracolumbar spinal cord, which synapse in the paravertebral ganglia (primarily the stellate and superior cervical ganglia) to send postganglionic fibers to the heart [StatPearls: Anatomy, Autonomic Nervous System]. The primary neurotransmitter released is norepinephrine, which activates beta-1 adrenergic receptors on cardiac myocytes to increase heart rate, contractility, and conduction velocity [NIH: Heart Physiology]. In pathological states like chronic heart failure and hypertension, the CSNS often becomes hyperactive, leading to adverse remodeling and an increased risk of lethal arrhythmias [PubMed: Sympathetic Nervous System in Heart Failure]. This system is a major focus of cardiovascular therapy, targeted through beta-blockers that inhibit catecholamine binding or interventional procedures like cardiac sympathetic denervation to reduce sympathetic drive and improve patient survival.
Antagonism of beta-1 and beta-2 adrenergic receptors; inhibition of norepinephrine release; depletion of catecholamine stores; surgical or percutaneous neuromodulation (denervation).
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