Linked Life Data

2090038

Source:http://linkedlifedata.com/resource/pubmed/id/2090038

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1991-5-28
pubmed:abstractText
Amitraz (N'-[2,4-dimethylphenyl]-N-[(2,4-dimethylphenyl)imino]-N- methylmethanimidamide) is a formamidine insecticide/acaricide that increases plasma glucose and decreases plasma insulin concentrations in dogs when applied topically. Because amitraz activates alpha 2-adrenoceptors in numerous tissues, in this study we used rats as a model to determine whether these effects of amitraz are mediated by alpha 2-adrenoceptors. The i.v. injection of amitraz (0.1, 0.3, and 1 mg/kg) followed by i.v. glucose injection (1 g/kg) induced a dose-dependent glucose intolerance characterized by hypoinsulinemia. At 1 mg/kg, amitraz completely blocked the insulin release induced by i.v. glucose administration. The alpha 2-adrenoceptor antagonist yohimbine (1 mg/kg, i.v.) prevented the effects of amitraz, but the alpha 1-adrenoceptor antagonist prazosin (0.3 mg/kg, i.v.) did not. The results suggested that one mechanism by which amitraz prolongs glucose-induced hyperglycemia is via inhibition of insulin release and this effect is mediated by alpha 2-adrenoceptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0340-5761
pubmed:author
pubmed:issnType
Print
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
680-3
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Amitraz-induced glucose intolerance in rats: antagonism by yohimbine but not by prazosin.
pubmed:affiliation
Department of Veterinary Physiology and Pharmacology, Iowa State University, Ames 50011.
pubmed:publicationType
Journal Article