The interaction of choline esters, vagal stimulation and H2-receptor blockade on acid secretion in vitro.
Choline esters, bethanechol and carbachol, and electrical field stimulation increased acid secretion in the mouse, isolated, lumen-perfused, stomach. Electrical field stimulation was apparently mediated by vagal nerve ending because treatment with either tetrodotoxin or atropine abolished the response. Using a 2 + 2 assay design, experiments with bethanechol showed that the H2-receptor antagonists metiamide and cimetidine (1 mM) were devoid of antimuscarinic activity. However, the effects of carbachol, which unlike bethanechol stimulates both muscarinic and nicotinic receptors, were significantly antagonised by metiamide (1 mM) at a concentration which was not anticholinergic. We conclude that there are cholinergic receptors separate from histamine H2-receptors on parietal cells. The effects of vagal stimulation in this preparation however, are apparently mediated by histamine release. These results support the "two-cell hypothesis' where vagal nerve endings synapse with the parietal cell.
D000818:Animals; D001626:Bethanechol Compounds / Q000494:pharmacology*; D002217:Carbachol / Q000494:pharmacology*; D004558:Electric Stimulation; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D006635:Histamine H2 Antagonists / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D011976:Receptors, Muscarinic / Q000187:drug effects; D014630:Vagus Nerve / Q000502:physiology*
D001626:Bethanechol Compounds; D006635:Histamine H2 Antagonists; D011976:Receptors, Muscarinic; D002217:Carbachol