Source:http://linkedlifedata.com/resource/pubmed/id/15258766
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2004-12-3
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pubmed:abstractText |
This study investigated the effects of changing the extracellular [Mg(2+)] ([Mg(2+)](o)) on endothelin-1 (ET-1)-induced contraction of rabbit coronary artery smooth muscle and the involvement of non-selective cation (NSC) channels in this response. Increased [Mg(2+)](o) shifted the concentration/contraction relationship curve of ET-1 to the right. In whole-cell patch clamp recordings, ET-1 (10(-7) M) induced a long-lasting inwards current (94.7+/-7.2 pA) that was inhibited by 8 mM [Mg(2+)](o) (45.3+/-4.4%) and NSC channel blockers (10(-3) M streptomycin and 10(-3) M La(3+)), but not by the voltage-dependent Ca(2+) channel blocker nicardipine. The current/voltage (I/V) curve was linear. Furthermore, in pressurized arteries, the ET-1-induced contraction was also inhibited by La(3+) and streptomycin, but not by nicardipine. U-73122, a selective phospholipase C (PLC) inhibitor and staurosporine and GF 109203X, which block protein kinase C (PKC), reduced ET-1-activated NSC currents by 54.2+/-5.1%, 60.3+/-5.5% and 48.5+/-2.9%, respectively. The inwards current was increased by 1-oleoyl-2-acetyl-sn-glycerol (OAG) and phorbol 12,13-dibutyrate (PDBu), which activate PKC selectively. Like transient receptor potential channel (TRPC3) currents, ET-1-activated NSC currents had a linear I/V relationship, were blocked by flufenamate and activated by a diacylglycerol analogue. These results suggest that [Mg(2+)](o) blocks ET-1-induced contraction of coronary arteries by inhibiting NSC channels. Activation of PLC and PKC might be involved in activation of NSC channels.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cations,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Magnesium,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Type C Phospholipases
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0031-6768
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
449
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
195-204
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:15258766-Animals,
pubmed-meshheading:15258766-Cations,
pubmed-meshheading:15258766-Coronary Vessels,
pubmed-meshheading:15258766-Endothelin-1,
pubmed-meshheading:15258766-Extracellular Space,
pubmed-meshheading:15258766-Female,
pubmed-meshheading:15258766-Ion Channel Gating,
pubmed-meshheading:15258766-Ion Channels,
pubmed-meshheading:15258766-Magnesium,
pubmed-meshheading:15258766-Male,
pubmed-meshheading:15258766-Membrane Potentials,
pubmed-meshheading:15258766-Muscle, Smooth, Vascular,
pubmed-meshheading:15258766-Muscle Contraction,
pubmed-meshheading:15258766-Patch-Clamp Techniques,
pubmed-meshheading:15258766-Protein Kinase C,
pubmed-meshheading:15258766-Rabbits,
pubmed-meshheading:15258766-Type C Phospholipases
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pubmed:year |
2004
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pubmed:articleTitle |
Extracellular Mg(2+) blocks endothelin-1-induced contraction through the inhibition of non-selective cation channels in coronary smooth muscle.
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pubmed:affiliation |
Department of Physiology and National Research Laboratory for Cellular Signalling, Seoul National University College of Medicine, 28 Yonkeun-Dong, Chongno-Ku, 110-799 Seoul, Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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