Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5-6
pubmed:dateCreated
1996-12-30
pubmed:abstractText
Pharmacological characteristics of [3H]taurine release evoked by nitric oxide (NO) were investigated using mouse cerebral cortical neurons in primary culture. NO generators such as S-nitroso-N-acetylpenicillamine (SNAP) and sodium nitroprusside (SNP) dose-dependently increased [3H]taurine release from neurons. Such stimulatory effects of NO generators were completely abolished by hemoglobin, a NO radical scavenger, indicating that these [3H]taurine releases might be due to NO liberated from SNAP and SNP. Sodium withdrawal from incubation buffer significantly inhibited the SNAP- and SNP-induced [3H]taurine releases, whereas the removal of calcium showed no alterations in the [3H]taurine release evoked by NO generators. Beta-Alanine and guanidinoethane sulfonate, inhibitors of carrier-mediated taurine transport system, inhibited the SNAP- and SNP-evoked releases of [3H]taurine in a dose-dependent manner. These results indicate that the NO-evoked [3H]taurine release from cerebral cortical neurons is mediated by the reverse process of sodium-dependent carrier-mediated taurine transport system.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0197-0186
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
601-7
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:articleTitle
Characteristics of nitric oxide-evoked [3H]taurine release from cerebral cortical neurons.
pubmed:affiliation
Department of Pharmacology, Kyoto Prefectural University of Medicine, Japan.
pubmed:publicationType
Journal Article