Linked Life Data

18437094

Source:http://linkedlifedata.com/resource/pubmed/id/18437094

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-5-22
pubmed:abstractText
Mitochondrial (m) KATP channel opening has been implicated in triggering cardiac preconditioning. Its consequence on mitochondrial respiration, however, remains unclear. We investigated the effects of two different KATP channel openers and antagonists on mitochondrial respiration under two different energetic conditions. Oxygen consumption was measured for complex I (pyruvate/malate) or complex II (succinate with rotenone) substrates in mitochondria from fresh guinea pig hearts. One of two mKATP channel openers, pinacidil or diazoxide, was given before adenosine diphosphate in the absence or presence of an mKATP channel antagonist, glibenclamide or 5-hydroxydecanoate. Without ATP synthase inhibition, both mKATP channel openers differentially attenuated mitochondrial respiration. Neither mKATP channel antagonist abolished these effects. When ATP synthase was inhibited by oligomycin to decrease [ATP], both mKATP channel openers accelerated respiration for both substrate groups. This was abolished by mKATP channel blockade. Thus, under energetically more physiological conditions, the main effect of mKATP channel openers on mitochondrial respiration is differential inhibition independent of mKATP channel opening. In contrast, under energetically less physiological conditions, mKATP channel opening can be evidenced by accelerated respiration and blockade by antagonists. Therefore, the effects of mKATP channel openers on mitochondrial function likely depend on the experimental conditions and the cell's underlying energetic state.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/5-hydroxydecanoic acid, http://linkedlifedata.com/resource/pubmed/chemical/Decanoic Acids, http://linkedlifedata.com/resource/pubmed/chemical/Diazoxide, http://linkedlifedata.com/resource/pubmed/chemical/Electron Transport Complex I, http://linkedlifedata.com/resource/pubmed/chemical/Electron Transport Complex II, http://linkedlifedata.com/resource/pubmed/chemical/Glyburide, http://linkedlifedata.com/resource/pubmed/chemical/Hydroxy Acids, http://linkedlifedata.com/resource/pubmed/chemical/Mitochondrial Proton-Translocating..., http://linkedlifedata.com/resource/pubmed/chemical/Pinacidil, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channel Blockers, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, http://linkedlifedata.com/resource/pubmed/chemical/mitochondrial K(ATP) channel
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
483-91
pubmed:dateRevised
2010-12-30
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
KATP channel openers have opposite effects on mitochondrial respiration under different energetic conditions.
pubmed:affiliation
Anesthesiology Research Laboratories, Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA. mriess@mcw.edu
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural