Linked Life Data

9074763

Source:http://linkedlifedata.com/resource/pubmed/id/9074763

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1997-5-27
pubmed:abstractText
The regulation of gastric acid secretion is achieved in the periphery by interplay between three major gastric endocrine cells: the enterochromaffin-like (ECL) cell, the gastrin or G cell, and the somatostatin or D cell. Regulation of these cells is via stimulatory or inhibitory paracrine, endocrine, and neural pathways. Upregulation of ECL function is determined by activation of CCK-B receptors, by gastrin, and by activation of beta-adrenergic receptors, as well as by acetylcholine in some (10-29%) of the cells. Gastrin and acetylcholine produce typical biphasic calcium signals. Inhibition of ECL cell histamine release and calcium signaling is produced by somatostatin acting at a type 2 receptor, histamine acting at a histamine-3 receptor, and by peptide PYY. Stimulation of ECL cells results in activation of chloride channels, and there is evidence that voltage-dependent calcium channels, along with the receptor-operated calcium channels, also are responsible for elevation of [Ca]i. Depolarization-activated K+ channels presumably restore the potential after depolarization by activation of the chloride channel. The D cell is activated by either gastrin or CCK and appears to be inhibited by acetylcholine and somatostatin. The G cell is activated by acetylcholine and gastrin-releasing peptide (GRP) and is inhibited by somatostatin. The functional integration of these three cell types is the primary determinant of the degree of stimulation of the parietal cell.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0066-4278
pubmed:author
pubmed:issnType
Print
pubmed:volume
59
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
243-56
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Physiology of isolated gastric endocrine cells.
pubmed:affiliation
Department of Medicine, University of California, Los Angeles 90073, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, Non-U.S. Gov't