Vagal cholinergic nerves

The vagus nerve is a major connection between central and peripheral components. It contains both afferent (80%) and efferent (20%) pathways from and to the upper GIT. These include both cholinergic and non-cholinergic nerve fibres the non-cholinergic neurones may have serotonin as transmitter. Two types of vagal afferent receptors are involved in the emetic response (1) mechanoreceptors, iocated in the muscular wall of the distal stomach and proximal duodenum, which are activated by distension or contraction of the gut wall and (2) chemoreceptors located in the gut mucosa of the upper small bowel. These monitor the... 

The parasympathetic nervous system, through the vagus nerve, inhibits the spontaneous rate of depolarization of pacemaker cells. The release of acetylcholine from cholinergic vagal fibers increases potassium conductance (gK+) in pacemaker cells, and this enhanced outward movement of K+ results in a more negative po-... 

As noted previously, the airways are richly supplied with afferent and efferent vagal nerves. The cholinergic motor fibers are clearly responsible in some patients for a portion of the bronchoconstriction characteristic of acute asthma. Such fibers innervate M3 receptors on the smooth muscle and contain modulatory M2 receptors on the nerve terminals. Selective inhibition of M2 receptors can increase bronchoconstrictor responses to a variety of stimuli, while M3 inhibitors can produce dilation of constricted airways. 

The cholinergic, i.e. parasympathetic system, acts through the vagal nerves by release of acetylcholine (ACh) that opposes the sympathetic stimulation. Parasympathetic preganghonic neurons originate in the medulla. Parasympathetic fibers terminate mainly on cells of the atria. Parasympathetic irmervation is denser in the SA and AV nodes than the left ventricle. The right vagus nerve innervates the SA node. The neurotransmitter ACh and adenosine promote susceptibility to atrial fibrillation, and shorten atrial refractoriness. Excessive stimulation causes bradyarrhythmia. The... 

Perhaps the most widely knowm agent to alter cholinergic transmission is the belladonna alkaloid, atropine. This agent is relatively selective for muscarinic receptors and as such decreases exocrine gland secretion, smooth muscle tone and the effects of vagal nerve stimulation of the heart. Atropine has several clinical applications including use as a preoperative medication, post-myocardial infarction to increase heart... 

Cannabinoids also inhibit transmitter release from cholinergic autonomic neurons (Table 4). As an example, the bradycardia elicited by vagal nerve stimulation is depressed. Figure 5B shows that cannabinoids inhibit parasympathetic neuroeffector transmission in the heart. Electrically evoked contractions of the ileum and urinarybladder can also be inhibited by activation of CBi receptors (Table 4). 

Although the effect is smaller than that observed in the atrium, ACh produces a negative inotropic effect in the ventricle. This inhibition is most apparent when there is concomitant adrenergic stimulation or underlying sympathetic tone. ACh suppresses automaticity of Purkinje fibers and increases the threshold for ventricular fibrillation. To the extent that the ventricle receives cholinergic innervation, sympathetic and vagal nerve terminals lie in close proximity, and muscarinic receptors are believed to exist at presynaptic as well as postsynaptic sites. 

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