Linked Life Data

16188348

Source:http://linkedlifedata.com/resource/pubmed/id/16188348

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-12-14
pubmed:abstractText
Uptake of K+ is an important role of astrocytes to maintain physiological lower extracellular K+ concentration in the CNS. In this study, the effect of high K+ concentration was examined on the cellular function of astrocytes from embryonic rat brain in primary culture. Nitric oxide (NO) production induced by lipopolysaccharide (LPS) was measured as an index of cellular function of astrocytes. Increasing KCl concentration to about 40 mM did not directly evoke NO production, but doubled the level of LPS (1 ng/ml)-induced NO production. K-gluconate showed a similar enhancing effect although the degree of enhancement was about half of that of KCl. Neither NaCl nor Na-gluconate showed any effect. The K(+)-channel blocker, 4-aminopyridine, but not tetraethylammonium or apamin, inhibited the enhancing effect of KCl. The LPS-induced iNOS protein expression determined by immunoblotting analysis was enhanced by high K+ treatment. The level of iNOS mRNA determined by real-time RT-PCR technique was also augmented by the presence of 40 mM KCl. These results indicate that the elevation of extracellular K+ concentration regulates astrocytic cell functions through a mechanism involving K(A)-type K(+)-channels and that potentiation of NO production by high K+ is due to the augmentation of iNOS mRNA and iNOS protein levels.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0197-0186
pubmed:author
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
43-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Potentiation by high potassium of lipopolysaccharide-induced nitric oxide production from cultured astrocytes.
pubmed:affiliation
Laboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, Sakai, Osaka 599-8531, Japan. yoichi@vet.osakafu-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't