Physiology and pathology of gastrin.
Gastrin release does play a part in the cephalic phase of acid secretion in man and is the major mechanism for the gastric phase of acid secretion. The vagal control of gastrin release is most likely mediated by cholinergic and possibly non-cholinergic excitatory fibres, as well as by cholinergic inhibitory fibres. Gastric luminal control of gastrin release is by local food and possibly distension stimulation, as well as by acid inhibition. Of the various causes of hypergastrinaemia, those associated with gastrinoma, G-cell hyperfunction and retained antrum have definite pathogenetic roles. Duodenal ulcer disease is a heterogeneous goup of disorders having different pathogenetic mechanisms. Parietal cell hyperplasia and G-cell dysfunctions, consisting of modest to florid G-cell hyperfunction and hyperplasia with secondary parietal cell hyperplasia, are but some facets of abnormalities that we have been able to identify.
D005750:Gastric Juice / Q000502:physiology; D005753:Gastric Mucosa / Q000294:innervation / Q000378:metabolism; D005755:Gastrins / Q000097:blood / Q000502:physiology*; D006801:Humans; D006965:Hyperplasia / Q000503:physiopathology; D010437:Peptic Ulcer / Q000503:physiopathology; D011706:Pyloric Antrum / Q000294:innervation / Q000378:metabolism / Q000473:pathology; D014630:Vagus Nerve / Q000502:physiology; D015043:Zollinger-Ellison Syndrome / Q000503:physiopathology
D005755:Gastrins