Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
25
pubmed:dateCreated
1998-1-14
pubmed:abstractText
Chloroethylclonidine increased cytosol [Ca2+] in rat-1 fibroblasts stably expressing alpha1a-adrenoceptors. The effect of the imidazoline was dose-dependent with a maximal effect (approximately 3-fold increase in [Ca2+]i) at 10 microM and it was blocked by phentolamine and 5-methyl urapidil, indicating that it was mediated through alpha1-adrenoceptors. Noradrenaline (1 microM) induced a much bigger effect (approximately 6-8-fold) in the same cells. When chloroethylclonidine was added before noradrenaline a dose-dependent inhibition of the effect of the natural catecholamine was observed. Chloroethylclonidine did not modified cytosol [Ca2+] in rat-1 fibroblast expressing alpha1b- or alpha1d-adrenoceptors. However, the imidazoline acutely inhibited the effect of noradrenaline in these cells. It is concluded that chloroethylclonidine interacts with alpha1a-adrenoceptors as a partial agonist inducing Ca2+ mobilization in a very short time frame and that it is able to inhibit the action of noradrenaline when co-incubated with the catecholamine in cells expressing any of the three alpha1-adrenoceptor subtypes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
PL 391-5
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Chloroethylclonidine is a partial alpha1A-adrenoceptor agonist in cells expressing recombinant alpha1-adrenoceptor subtypes.
pubmed:affiliation
Departamento de Farmacología y Toxicología, CINVESTAV-IPN, México, D.F., México.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't