Sympathetic nerve fibers to the liver derive from T7–T10.
Parasympathetic nerve fibers to the liver derive from the abdominal vagus nerve.
Postganglionic noradrenergic sympathetic nerve fibers end directly to hepatocytes and norepinephrine released from these nerve fibers initiates glycogenolysis and hyperglycemia and induces gluconeogenesis.
Autonomic innervation helps to regulate vascular, secretory, and phagocytic processes in the liver.
The gallbladder, especially the sphincter ampullae and the sphincter of the choledochal duct, is also supplied by autonomic nerve fibers.
The sympathetic nerve fibers cause contraction of the sphincters and dilation of the gallbladder.
The parasympathetic nerve fibers cause opening of the sphincters and contraction of the gallbladder.
Chronic activation of the sympathetic nervous system, with increased secretion of norepinephrine, can drive glucose levels, provoke insulin secretion, increase free-radical formation, increase platelet aggregation, and initiate other actions that are beneficial in an emergency but problematic when present chronically.
These connections may be one route by which chronic stressors intersect with metabolic syndrome, diminish antiviral and antitumor immunity, and increase the risk for a variety of chronic diseases, including hypertension, cardiovascular disease and stroke, some cancers, and type II diabetes.
Autonomic neuropathy to the gallbladder can result in atonic smooth muscle responses, with the development of gallstones (especially in individuals with hypercholesterolemia) and diarrhea.