Linked Life Data

7969782

Source:http://linkedlifedata.com/resource/pubmed/id/7969782

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1994-12-23
pubmed:abstractText
The involvement of hypothalamic histaminergic neurons in the mediation of the ACTH and beta-endorphin (beta-END) response to lipopolysaccharide (LPS) endotoxin was investigated in conscious male rats. LPS stimulated the release of ACTH and beta-END dose-dependently and increased the hypothalamic concentration of the histamine (HA) metabolite tele-methylhistamine significantly and that of HA slightly, indicating an increased turnover of neuronal HA. Pretreatment with the HA synthesis inhibitor alpha-fluoromethyl-histidine administered intracerebroventricularly (i.c.v.) or intraperitoneally (i.p.) inhibited the ACTH and beta-END response to LPS about 60%, whereas i.p. administration of the H3 receptor agonist R(alpha)methylHA, which inhibits HA synthesis and release, decreased the response about 50%. Pretreatment with the H1 receptor antagonist mepyramine (67 micrograms x 2 i.c.v.) inhibited the hormone response to LPS about 50%, while pretreatment with equimolar doses of the H2 receptor antagonists cimetidine (67 micrograms x 2 i.c.v.) or ranitidine (83 micrograms x 2 i.c.v.) had no effect on the LPS-induced release of ACTH and beta-END. When the H1 receptor antagonists mepyramine and cetirizine were administered i.p. in doses (10 mg/kg) which penetrate the blood-brain barrier the hormone response to LPS was inhibited 50% and 30%, respectively. Administered i.p. the H2 receptor antagonists had no effect on the hormone response to LPS. We conclude that hypothalamic histaminergic neurons in rats are involved in the mediation of the ACTH and beta-END response to LPS stimulation via activation of central postsynaptic H1 receptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Adrenocorticotropic Hormone, http://linkedlifedata.com/resource/pubmed/chemical/Endotoxins, http://linkedlifedata.com/resource/pubmed/chemical/Histamine, http://linkedlifedata.com/resource/pubmed/chemical/Histamine H1 Antagonists, http://linkedlifedata.com/resource/pubmed/chemical/Histamine H2 Antagonists, http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides, http://linkedlifedata.com/resource/pubmed/chemical/Methylhistamines, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Histamine H1, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Histamine H2, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Histamine H3, http://linkedlifedata.com/resource/pubmed/chemical/beta-Endorphin, http://linkedlifedata.com/resource/pubmed/chemical/tele-methylhistamine
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0028-3835
pubmed:author
pubmed:issnType
Print
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
243-51
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Role of hypothalamic histaminergic neurons in mediation of ACTH and beta-endorphin responses to LPS endotoxin in vivo.
pubmed:affiliation
Department of Medical Physiology, Panum Institute, University of Copenhagen, Denmark.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't