Source:http://linkedlifedata.com/resource/pubmed/id/19894035
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
|
pubmed:dateCreated |
2010-1-21
|
pubmed:abstractText |
Monosialotetrahexosylganglioside (GM1) is a glycosphingolipid present in most cell membranes that displays antioxidant and neuroprotective properties. It has been recently described that GM1 induces pial vessel vasodilation and increases NO( x ) content in cerebral cortex, which are fully prevented by the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). However, it is not known whether GM1 relaxes larger vessels, as well as the mechanisms by which GM1 causes vasorelaxation. In this study, we demonstrate that GM1 (10, 30, 100, 300 microM, 1 and 3 mM) induces vascular relaxation determined by isometric tension studies in rat mesenteric artery rings contracted with 1 microM phenylephrine. The vasorelaxation induced by GM1 was abolished by endothelium removal, by incubation with L-NAME (1 microM), and partially inhibited by the blockade of potassium channels by 1 mM tetraethylammonium, 10 microM glibenclamide, by the soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one (10 microM), and by 50 nM charybdotoxin, a blocker of large and intermediate conductance calcium-activated potassium channels. Moreover, GM1-induced relaxation was not affected by apamin (50 nM), a small conductance calcium-activated potassium channel blocker. The results indicate that direct and indirect nitric oxide pathways play a pivotal role in vasorelaxation induced by GM1, which is mediated mainly by potassium channels activation. We suggest that vasodilation may underlie some of the biological effects of exogenous GM1 ganglioside.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/G(M1) Ganglioside,
http://linkedlifedata.com/resource/pubmed/chemical/Guanylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Vasodilator Agents
|
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
1432-1912
|
pubmed:author | |
pubmed:issnType |
Electronic
|
pubmed:volume |
380
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
487-95
|
pubmed:meshHeading |
pubmed-meshheading:19894035-Animals,
pubmed-meshheading:19894035-Dose-Response Relationship, Drug,
pubmed-meshheading:19894035-G(M1) Ganglioside,
pubmed-meshheading:19894035-Guanylate Cyclase,
pubmed-meshheading:19894035-Male,
pubmed-meshheading:19894035-Mesenteric Arteries,
pubmed-meshheading:19894035-Nitric Oxide,
pubmed-meshheading:19894035-Potassium Channels,
pubmed-meshheading:19894035-Rats,
pubmed-meshheading:19894035-Rats, Wistar,
pubmed-meshheading:19894035-Vasodilation,
pubmed-meshheading:19894035-Vasodilator Agents
|
pubmed:year |
2009
|
pubmed:articleTitle |
Nitric oxide and potassium channels mediate GM1 ganglioside-induced vasorelaxation.
|
pubmed:affiliation |
Departamento de Fisiologia e Farmacologia, Universidade Federal de Santa Maria, Santa Maria, Rio Grande do Sul, Brazil.
|
pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
|