Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1982-12-16
pubmed:abstractText
Thymoxamine and deacetylthymoxamine antagonized the hypertensive response of pithed rats to noradrenaline and clonidine, probably by inhibiting vascular post-synaptic alpha-adrenoceptors. N-demethyl-deacetylthymoxamine was inactive. Clonidine-induced reduction of tachycardia caused by electrical stimulation of the cardiac sympathetic nerve in pithed rats was antagonized by phentolamine but not by prazosin, thymoxamine, deacetylthymoxamine or N-demetyldeacetylthymoxamine. This suggests that prazosin and thymoxamine and its derivatives predominantly blocked alpha 1-adrenoceptors. In pentobarbitone-anaesthetized normotensive rats, prazosin, thymoxamine and deacetylthymoxamine decreased the hypotensive effect of clonidine, but had no significant effect on clonidine-induced bradycardia. These substances antagonized clonidine-induced hypotension in rats by the probable mechanism of inhibiting central alpha 1-adrenoceptors whose characteristics are similar to peripheral receptors. These data suggest that clonidine produced a hypotensive action in pentobarbitone anaesthetized rats via alpha 1-adrenoceptors and produced bradycardia via alpha 2-adrenoceptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0301-4533
pubmed:author
pubmed:issnType
Print
pubmed:volume
258
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
116-27
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
Effects of thymoxamine and its metabolites on clonidine-induced hypotension and bradycardia in rats.
pubmed:publicationType
Journal Article