Editing Vagus nerve (section)

=== Cardiac effects ===
[[File:Sinoatrial node high mag.jpg|thumb|[[H&E stain]]ed fibers of the vagus nerve (bottom right) innervate the [[sinoatrial node]] tissue (middle left)]]

Parasympathetic innervation of the heart is partially controlled by the vagus nerve and is shared by the [[thoracic ganglia]]. Vagal and spinal ganglionic nerves mediate the lowering of the [[heart rate]]. The right vagus branch innervates the [[sinoatrial node]]. In healthy people, parasympathetic tone from these sources is well-matched to sympathetic tone. Hyperstimulation of parasympathetic influence promotes [[bradyarrhythmias]]. When hyperstimulated, the left vagal branch predisposes the heart to [[heart block|conduction block]] at the [[atrioventricular node]].

At this location, neuroscientist [[Otto Loewi]] first demonstrated that nerves secrete substances called [[neurotransmitters]], which have effects on receptors in target tissues. In his experiment, Loewi electrically stimulated the vagus nerve of a frog heart, which slowed the heart. Then he took the fluid from the heart and transferred it to a second frog heart without a vagus nerve. The second heart slowed without electrical stimulation. Loewi described the substance released by the vagus nerve as [[vagusstoff]], which was later found to be [[acetylcholine]]. 

Drugs that inhibit the [[muscarinic receptor]]s ([[anticholinergic]]s) such as [[atropine]] and [[Hyoscine hydrobromide|scopolamine]], are called vagolytic because they inhibit the action of the vagus nerve on the heart, gastrointestinal tract, and other organs.  Anticholinergic drugs increase heart rate and are used to treat [[bradycardia]].