Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1993-1-4
pubmed:abstractText
The uptake of [3H]5-hydroxytryptamine (5-HT) in bovine cerebral arteries was reduced by cocaine (1 microM), ouabain (100 microM), pretreatment with 6-hydroxydopamine (6-OHDA) (1.46 mM, 10 min) and metitepine (1 microM). Electrically-stimulated tritium release was decreased by tetrodotoxin (0.8 microM), Ca-free medium, denervation with 6-OHDA (1.46 mM, 10 min), 5-HT (10 microM), noradrenaline (1 microM) and the agonist of alpha 2-adrenoceptors B-HT 920 (0.1 and 1 microM), enhanced by metitepine (1 microM, antagonists of presynaptic 5-HT1 receptors) and rauwolscine (1 microM, antagonist at alpha 2-adrenoceptors, and also of 5-HT1D receptors) and not affected by ketanserin (1 microM, antagonist of 5-HT2 receptors), methysergide (0.1 microM, antagonist of 5-HT1 and 5-HT2 receptors) and phentolamine (1 and 3 microM antagonist of alpha-adrenoceptors and less potent of 5-HT1 receptors). The inhibitory action of 10 microM 5-HT was partially reversed by phentolamine (3 microM) and cocaine (1 microM) and completely reversed by both metitepine (1 microM) and rauwolscine (1 microM). Ketanserin (1 microM), methysergide (0.1 microM) or phentolamine (1 microM) had no effect. Rauwolscine (1 microM) antagonized the inhibition induced by both noradrenaline (1 microM) and B-HT 920 (0.1 and 1 microM). 5-HT induced tritium release which was inhibited by cocaine (an antagonist of 5-HT3 receptors) and denervation with 6-OHDA.(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-3573
pubmed:author
pubmed:issnType
Print
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
824-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Receptors involved in the modulation of 5-hydroxytryptamine release in bovine cerebral arteries.
pubmed:affiliation
Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Madrid, Spain.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't