ArticleThe Journal of physiology1993
Enhancement by atropine of the pancreatic exocrine secretions evoked by vagal stimulation in the pithed rat.
Article in The Journal of physiology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 6 citations in OpenAlex.
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Pancreatic secretions were collected in response to 15 min periods of bilateral stimulation of the cervical vagus nerves in the pithed rat. 2. The weight of juice, total HCO3- and total protein evoked by a second period of vagal stimulation were essentially similar to those of the first period of vagal stimulation. 3. When the second period of vagal stimulation was preceded by an intravenous bolus injection of atropine sufficient to block the vagally induced bradycardia, the weight of secretion and total protein were greatly potentiated over an extended time course far exceeding that of the period of vagal stimulation. Total HCO3- was unchanged. 4. By contrast, atropine was effective in antagonizing the stimulatory effects of the muscarinic agonist methacholine injected intravenously. 5. The putative VIP (vasoactive intestinal polypeptide) antagonist [D-p-chloro-Phe6, Leu17]-VIP injected intravenously also increased the vagally evoked weight of juice, with total HCO3- and total protein unchanged. This was explicable by a partial agonist effect which was additive to the stimulatory action of vagal stimulation. 6. To explain these results, it is proposed that endogenously released acetylcholine exerts a negative feedback effect on the postganglionic varicosities which release both acetylcholine and another cotransmitter which was not excluded as being VIP. In the presence of atropine, the cotransmitter is proposed to be released from the inhibitory feedback, thus enhancing the response to vagal stimulation.
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