Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1984-2-14
pubmed:abstractText
This study was performed to elucidate mechanisms responsible for the contraction of isolated canine cerebral arteries induced by uridine 5'-triphosphate (UTP) and to ascertain whether UTP given intracisternally causes cerebral arterial constriction. The latter was proven arteriographically to be the case. In vitro, UTP (10(-4)M) and UDP were similar in potency, produced sustained contractions, and were more effective than other pyrimidine nucleotides or uridine. Unlike serotonin (5-HT), UTP was not antagonized by cinanserin and failed to cause constriction of mesenteric arteries. Adenosine similarly antagonized 5-HT and UTP. The Ca2+ antagonist nimodipine abolished contractions caused by high K+ but only incompletely antagonized 5-HT or UTP. On the other hand, procedures that hyperpolarize the cell membrane (low K+ followed by K+) abolished tonic contractions induced by UTP. Hyperpolarization prior to UTP (with or without nimodipine) did not, however, prevent the occurrence of a phasic contraction. Papaverine or lanthanum antagonized this phasic response. It was concluded that UTP selectively affects cerebral arteries, may initiate contraction by releasing membrane bound Ca2+, depolarizes the cell membrane to open receptor operated and potential sensitive calcium channels, but does not inhibit the electrogenic Na-pump nor specifically antagonize the vasodilator adenosine.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0039-2499
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
347-55
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:articleTitle
Mechanisms of the contractile effect induced by uridine 5-triphosphate in canine cerebral arteries.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't