Linked Life Data

6192725

Source:http://linkedlifedata.com/resource/pubmed/id/6192725

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1983-9-20
pubmed:abstractText
The action of natural and synthetic somatostatin-(1--28), [Nle8]somatostatin-(1--28), somatostatin-(15--28), and somatostatin-(1--14) was examined in dispersed acini from guinea pig pancreas. At high concentrations, the 28-amino acid form of somatostatin increased amylase release, outflux of 45Ca, cellular cGMP, and to a lesser extent cellular cAMP. The increase in amylase release was suppressed by dibutyryl cGMP but was not modified by theophylline or atropine. Binding of 125I-labeled [Thr28, Nle31] cholecystokinin-(25--33) was inhibited by [Nle8]somatostatin-(1--28). These effects required the entire 28-amino acid peptide and appeared to result from occupation of cholecystokinin receptors. It is postulated that they involve interactions between the C-terminal and the N-terminal sequences of the molecule with the participation of the amino acid in position 8. At low concentrations, natural and synthetic forms of somatostatin-(1--28) and somatostatin-(15--28) inhibited secretin- and vasoactive intestinal peptide (VIP)-stimulated increases in cellular cAMP concentration. No difference was found between the potency of somatostatin peptides, indicating that the tetradecapeptide somatostatin-(15--28) is sufficient to exert an inhibitory action on secretin- and VIP-stimulated cellular cAMP concentration. By contrast, the somatostatin fragment S-(1--14) was inactive on pancreatic cellular function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
245
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
G208-16
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
Bimodal regulation of pancreatic exocrine function in vitro by somatostatin-28.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't