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Like the sympathetic nervous system (SNS), the parasympathetic nervous system (PSNS) also begins with unmyelinated preganglionic neurons and ends with myelinated postganglionic neurons. Parasympathetic preganglionic fibers leave the central nervous system (CNS) in both cranial and sacral nerves. Cranial fibers arise from specific parasympathetic brainstem motor nuclei of cranial nerves III, VII, IX, and X, traveling with the main body of fibers within the cranial nerves to ganglia that are generally distant to the CNS and close to the target organ. Sacral outflow originates in the intermediolateral gray horns of the second, third, and fourth sacral nerves.

Cranial nerve X (vagus) accounts for more than 75% of PSNS activity, innervating the heart, lungs, esophagus, stomach, small intestine, proximal half of the colon, liver, gall bladder, pancreas, and upper portions of the ureters. The sacral nerves form the pelvic visceral nerves, which supply the descending colon, rectum, uterus, bladder, and lower portions of the ureters.

In contrast to the SNS, preganglionic PSNS fibers are generally long and pass directly to the effector organ, whereas postganglionic fibers are short and are situated near or within the innervated viscera. The ratio of postganglionic to preganglionic neurons is also much smaller in the PSNS (3:1) when compared to the SNS (20:1). The decreased number of preganglionic to postganglionic synapses may explain the discrete and limited effect of PSNS, such as vagal bradycardia occurring without concomitant change in intestinal motility.


Parasympathetic effects are generally mediated by muscarinic acetylcholine (ACh) receptors, with termination of action due to ACh hydrolysis. Similar to adrenoreceptors, they are G protein-linked receptors classified as M1-M5. M1 receptors are found on gastric parietal cells stimulating acid secretion; M2 receptors are found in the heart and decrease the heart rate; M3 receptors contract smooth muscle in the gut; M4 receptors cause epinephrine (EPI) release from the adrenal medulla with SNS stimulation; and M5 receptors have a CNS effect that is not well understood.

In the heart, the PSNS fibers travel via the vagus nerve, which also contains some SNS fibers to primarily control chronotropy. The majority of cardiac PSNS fibers are distributed to the sinoatrial and atrioventricular nodes, with some distribution to the atria and very little distribution to the ventricles. Vagal stimulation leads to decreased sinoatrial (SA) node discharge and decreased atrioventricular (AV) excitability, ultimately leading to decreased ventricular conduction and bradycardia. The PSNS effect on contractility is relatively negligible compared to its profound chronotropic effects.

The lungs are also innervated by the PSNS via the vagus nerve. Pulmonary vasculature is poorly responsive to vagal stimulation, especially when compared to the SNS effect. However, vagal stimulation causes intense bronchoconstriction and bronchial secretion. Vagal stimulation in the alveolar ducts also controls the reflex regulation of the ventilatory cycle.

The PSNS ...

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