Linked Life Data

2253822

Source:http://linkedlifedata.com/resource/pubmed/id/2253822

Statements in which the resource exists.
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pubmed-article:2253822pubmed:abstractTextThe influence of cholinergic blockade as well as vagal denervation of the oxyntic gland mucosa on the gastrin response to gastrin-releasing peptide (GRP) have been studied in patients with duodenal ulcer disease. The gastric luminal content was neutralized during the experiments. GRP induced a substantial increase in gastrin levels with a peak response already after 15 min of infusion. Vagal denervation of the parietal cell area induced a significant increase in basal gastrin concentrations and a significant enhancement of the GRP response. Two different doses of benzilonium bromide were studied and neither influenced the basal concentrations of gastrin. A significantly increased gastrin response to GRP was, however, observed after administration of both a high and a very low dose of the anticholinergic drug. Our results delineate a vagal, noncholinergic inhibitory influence on the basal gastrin release. In addition a vagally dependent oxyntopyloric mechanism inhibits the gastrin release stimulated by GRP. This inhibitory mechanism may hypothetically be a cholinergic reflex mechanism.lld:pubmed
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pubmed-article:2253822pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:2253822pubmed:articleTitleEffect of parietal cell vagotomy and cholinergic blockade on gastrin release in man induced by gastrin-releasing peptide.lld:pubmed
pubmed-article:2253822pubmed:affiliationDepartment of Surgery, Sahlgren's Hospital, University of Gothenburg, Sweden.lld:pubmed
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pubmed-article:2253822pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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