Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-7-26
pubmed:abstractText
Interactions between neuropeptides contained in autonomic vasodilator neurons supplying the guinea pig uterine artery were investigated in isolated segments of the artery precontracted with prostaglandin F2 alpha. Neither somatostatin-14 (10(-6) mol.l-1) nor dynorphin A(1-17) (10(-6) mol.l-1) had direct effects on vascular tone, and did not affect relaxations produced by guinea pig vasoactive intestinal peptide (gpVIP). Both the porcine and the guinea pig forms of neuropeptide Y (NPY; 10(-7)-10(-5) mol.l-1) caused transient contraction of the precontracted arteries. NPY also inhibited relaxations of the artery produced by gpVIP, an action which was not directly related to the NPY contractions. NPY caused both a concentration-dependent rightward shift in the gpVIP concentration-response curve, and a reduction in size of the maximum relaxation to gpVIP. NPY (10(-6) mol.l-1) also produced a rightward shift in the concentration-response curves for the vasodilators forskolin and glyceryl trinitrate, but did not reduce the maximum relaxations to these compounds. Thus NPY, which is colocalized with VIP in vasodilator neurons supplying the uterine artery, can greatly reduce the vasodilator potency of VIP.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0196-9781
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
381-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Neuropeptide Y inhibits relaxations of the guinea pig uterine artery produced by VIP.
pubmed:affiliation
Centre for Neuroscience, School of Medicine, Flinders University of South Australia, Bedford Park.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't