Vagal and hormonal influences on gastric secretion in duodenal ulcer disease.
Current concepts on the pathophysiology of gastric hypersecretion in duodenal ulcer disease have been presented and the role of vagal nerves and gastrointestinal hormones particularly gastrin has been discussed. Duodenal ulcer patients form a heterogenous group with regard to the gastric acid and pepsin secretion and gastrin release. They may differ from healthy subjects by several wall defined defects including an increased mass of parietal and peptic cells, increased capacity to secrete acid and pepsin, increased vagal drive to the parietal cells, hyperreactivity of antrum, decreased effectiveness of antral and duodenal autoregulatory mechanisms, defective release of secretin, increased gastric emptying and defective removal of gastric acid load from the duodenum. Very little is known what proportion of duodenal ulcer patients suffer from various pathologic disturbences and what are the mechanisms underlying these changes.
D000818:Animals; D004381:Duodenal Ulcer / Q000503:physiopathology*; D005750:Gastric Juice / Q000378:metabolism*; D005753:Gastric Mucosa / Q000473:pathology; D005755:Gastrins / Q000378:metabolism; D005768:Gastrointestinal Hormones / Q000378:metabolism*; D006801:Humans; D006965:Hyperplasia; D011706:Pyloric Antrum / Q000378:metabolism; D051381:Rats; D014630:Vagus Nerve / Q000503:physiopathology*
D005755:Gastrins; D005768:Gastrointestinal Hormones