Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1986-7-14
pubmed:abstractText
Neuropeptide Y (NPY) infusions into isolated, perfused, spontaneously beating hearts of guinea pigs elicited concentration-dependent increases of myocardial perfusion pressure and decreases of myocardial tension, but no consistent changes of heart rate. The increase of perfusion pressure caused by NPY (attributed to a constrictor effect on coronary vessels) was not affected by atropine, prazosin, yohimbine, propranolol, cimetidine, diphenhydramine, indomethacin or a mixture of methysergide and morphine. However, it was reduced by verapamil, a Ca2+ antagonist. Deletion of the N-terminal amino acid Tyr1 from the NPY molecule caused a 12-fold reduction of NPY potency as a coronary constrictor. Further shortening of the NPY molecule by removal of sequence Tyr1 through Glu15 or Tyr1 through Ala18 caused major losses of potency without detectable reduction of intrinsic activity. The results suggest that the constrictor effect of NPY on guinea pig coronary vessels results from a direct effect on vascular smooth muscle cells, is mediated by specific receptors and is likely to involve the participation of extracellular calcium ions. The results also suggest that the chemical groups responsible for the vasoconstrictor effect of NPY in guinea pig hearts might be scattered in the C-terminal end of the peptide.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0196-9781
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
27-31
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
The vasoconstrictor effect of neuropeptide Y and related peptides in the guinea pig isolated heart.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, Non-U.S. Gov't