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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-12-3
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
449
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
195-204
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Extracellular Mg(2+) blocks endothelin-1-induced contraction through the inhibition of non-selective cation channels in coronary smooth muscle.
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.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't