Linked Life Data

12199147

Source:http://linkedlifedata.com/resource/pubmed/id/12199147

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2002-8-29
pubmed:abstractText
Strong evidence supports that nitric oxide (NO) alters cell signaling pathways involving arachidonic acid (AA). Little is known, however, about the reciprocal modulation of nitrergic pathways by AA. The effects of exogenous AA on signal transduction of M1 muscarinic acetylcholine receptors were investigated in a model system of stably transfected Chinese hamster ovary cells. AA concentration-dependently inhibited the effects of carbachol in producing NO (IC50 = 191 microM) but did not alter inositol phosphate production or M1 receptor binding. AA inhibited both carbachol-induced transient and sustained increase in intracellular calcium concentration ([Ca2+]i; IC50 = 11 and 12 microM, respectively). Furthermore, AA-induced increase in [Ca2+]i cross-desensitizes with thapsigargin, but AA does not inhibit Ca(2+)-ATPase activity. These data support the concept that AA concentration-dependently inhibits receptor-mediated NO production at the level of calcium mobilization.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0364-3190
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
441-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Arachidonic acid inhibition of muscarinic receptor-mediated nitric oxide production occurs at the level of calcium mobilization in Chinese hamster ovary cells.
pubmed:affiliation
Division of Neuroscience Research in Psychiatry, University of Minnesota, Minneapolis, Minnesota, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.