Carnell, Anthony James (1994) Non-cholinergic, vagally evoked gastric relaxation in the rat. University of Southampton, Doctoral Thesis.
Abstract
The vagus nerve exerts both excitatory and inhibitory influences over gastric smooth muscle tone. Excitatory influences are mediated by cholinergic preganglionic parasympathetic neurones which activate intramural ganglion cells through nicotinic ganglionic transmission. These latter neurones release acetylcholine which then acts at muscarinic receptors on gastric smooth muscle itself, causing it to contract.
Most investigations of vagally mediated gastric smooth muscle relaxation have concentrated on pathways resistant to muscarinic antagonists. These inhibitory pathways have generally been ascribed to the release of non-adrenergic, non-cholinergic inhibitory transmitters from intrinsic intramural neurones.
There is some, largely morphological, evidence that preganglionic parasympathetic vagal fibres may use other transmitters in addition to acetylcholine. Candidates include catecholamines, L-3,4-dihydroxyphenylalanine, 5-hydroxytryptamine and a variety of neuropeptides. This study represents an attempt to identify a role for such transmitters in vagally mediated gastric relaxation following nicotinic ganglion blockade.
The data in the present study suggest that there is an inhibitory non-cholinergic preganglionic parasympathetic vagal pathway to gastric smooth muscle which is resistant to both nicotinic and muscarinic receptor blockade. This non-cholinergic pathway appears to involve a catecholaminergic component and a nitroxergic component. The role of histamine, 5-hydroxytryptamine, prostaglandins, endogenous opioids and L-3,4-dihydroxyphenylalanine in this pathway is also examined. Such a non-cholinergic vagal influence is likely to play an important role in physiological phenomena such as the relaxation of the stomach that occurs in response to a meal or emetic stimuli.
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