Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5 Pt 1
pubmed:dateCreated
1984-6-20
pubmed:abstractText
Epidermal growth factor (EGF) has been reported to stimulate epithelial cell proliferation and to inhibit gastric H+ secretion, but no details of the latter effect have been studied. This paper reports the effects of EGF on gastric and pancreatic secretions induced by various stimulants in vivo on conscious dogs and in vitro on isolated rabbit gastric glands. EGF was found to be an effective inhibitor of H+ secretion induced from the fully innervated and vagally denervated portions of the stomach stimulated by secretagogues activating receptors of the parietal cells (pentagastrin, histamine, and urecholine) and by natural stimulants such as sham or ordinary feeding. It appears to act directly on the parietal cells, as the inhibitory effect in vivo was not accompanied by any change in postprandial serum gastrin level. In addition, EGF was found to suppress H+ formation in the isolated gastric glands, both under resting conditions and after stimulation with histamine, carbachol, or dibutyryl cAMP. EGF failed to affect pancreatic response to exogenous hormones (secretin and cholecystokinin) but reduced postprandial secretion probably because of inhibition of H+ secretion from the subsequent reduction in duodenal acid loads. We conclude that EGF is a potent, specific, and direct inhibitor of H+ secretion from the parietal cells and that it does not affect alkaline gastroduodenal or pancreatic secretion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
246
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
G580-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
Effects of epidermal growth factor on gastrointestinal secretions.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't