Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1989-3-1
pubmed:abstractText
Neuropeptide Y (NPY) inhibits electrogenic Cl secretion in rat jejunal epithelium under voltage clamp conditions. This effect is dependent upon endogenous eicosanoid formation since it is blocked by the cyclooxygenase inhibitor, piroxicam, which itself has an inhibitory action upon chloride secretion. A number of chloride secretagogues have been examined for their ability to restore the antisecretory effects of NPY. Data presented here shows that NPY responsiveness is restored, in piroxicam pretreated tissues, by vasoactive intestinal polypeptide (VIP), forskolin, prostaglandin E2 (PGE2) isobutyl-1-methyl-xanthine (IBMX) and dibutyryl cAMP added prior to the neuropeptide. While all these agents cause chloride secretion by elevating intracellular cAMP, NPY is also effective in inhibiting the secretory effects of carbachol (CCh) and substance P (SP), agents believed to act by raising intracellular calcium (Cai). Although there is evidence that NPY can inhibit adenylate cyclase, its ability to attenuate chloride secretion brought about by secretagogues acting through both adenylate cyclase and calcium mechanisms, implies that NPY has either a more general fundamental mechanism or has multiple interactions with different second messenger systems.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
413
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
38-42
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Neuropeptide Y antagonises secretagogue evoked chloride transport in rat jejunal epithelium.
pubmed:affiliation
Department of Pharmacology, University of Cambridge, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't