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Effects of atropine on secretion and motility in isolated gastric mucosa and attached muscularis externa from ferret and cat
Author(s) -
Roth S. H.,
Schofield B.,
Yates J. C.
Publication year - 1979
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1979.sp012855
Subject(s) - pentagastrin , atropine , cholinergic , medicine , endocrinology , acetylcholine , muscarinic acetylcholine receptor , secretion , gastric mucosa , gastric acid , chemistry , motility , parasympathomimetics , biology , stomach , receptor , microbiology and biotechnology
1. A combined in vitro preparation of gastric mucosa and adjacent muscle from young ferrets and kittens has been used to study the effects of atropine on acid secretion and motility produced by acetylcholine (ACh) and pentagastrin. 2. The minimal dose of atropine required to abolish a maximum secretory response to ACh also prevented the associated motility response. This dose of atropine also blocked the motility response to pentagastrin, but was without influence on the secretory effect of this agent. A 10 3 times larger dose of atropine reduced the secretory effect of pentagastrin by half, probably not by anti‐muscarinic effect. The results exclude the possibility that the acid secretory response to pentagastrin necessarily involves a cholinergic receptor. 3. The results support the view that the response of the fundic smooth muscle to pentagastrin depends on the excitation of cholinergic nerves. 4. No evidence has been found of any cholinergic component in the acid secretory response to pentagastrin. In assessing the significance of this result, however, it must be remembered that the Auerbach plexus has been removed over the major part of the mucosa, and the Meissner plexus deprived of input and probably damaged. 5. The results are compatible with the hypothesis that the depressant effect of atropine on acid secretion produced by gastrin and its derivatives is due to the elimination of a cholinergic potentiating influence arising in the intramural plexuses. The residual Meissner plexus elements in this in vitro preparation appear inadequate to sustain this effect.