Linked Life Data

8251426

Source:http://linkedlifedata.com/resource/pubmed/id/8251426

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1994-1-10
pubmed:abstractText
The vasodilating mechanisms of the K+ channel openers--cromakalim, pinacidil, nicorandil, KRN2391, and Ki4032--were examined by measurement of the cytoplasmic Ca2+ concentration ([Ca2+]i) using the fura-2 method in canine or porcine coronary arterial smooth muscle. The five K+ channel openers all produced a reduction of [Ca2+]i in 5 and 30 mM KCl physiological salt solution (PSS), the effects of which were antagonized by tetrabutylammonium (TBA) or glibenclamide, but failed to affect [Ca2+]i in 45 and 90 mM MCl-PSS. Cromakalim and Ki4032 only partially inhibited the 30 mM KCl-induced contractures, whereas pinacidil, nicorandil, and KRN2391 nearly abolished contractions produced by high KCl-PSS. The increased [Ca2+]i and force produced by a thromboxane A2 analogue, U46619, were inhibited by K+ channel openers and verapamil. In the absence of extracellular Ca2+, U46619 induced a transient increase in [Ca2+]i with a contraction, which is effectively inhibited by cromakalim and Ki4032. Their inhibitory effects were blocked by TBA and counteracted by 20 mM KCl-induced depolarization. Cromakalim and Ki4032 did not affect caffeine-induced Ca2+ release. Cromakalim reduced U46619-induced IP3 production and TBA blocked this inhibitory effect. Thus, cromakalim and Ki4032 are more specific K+ channel openers than pinacidil, nicorandil, and KRN2391. The vasodilation related with a reduction of [Ca2+]i produced by K+ channel openers is due to the hyperpolarization of the plasma membrane resulting in not only the closure of voltage-dependent Ca2+ channels but also inhibition of the production of IP3 and Ca2+ release from intracellular stores related to stimulation of the thromboxane A2 receptor.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0920-3206
pubmed:author
pubmed:issnType
Print
pubmed:volume
7 Suppl 3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
565-74
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8251426-15-Hydroxy-11 alpha,9..., pubmed-meshheading:8251426-Animals, pubmed-meshheading:8251426-Arteries, pubmed-meshheading:8251426-Calcium, pubmed-meshheading:8251426-Coronary Vessels, pubmed-meshheading:8251426-Dogs, pubmed-meshheading:8251426-Female, pubmed-meshheading:8251426-Fluorescence, pubmed-meshheading:8251426-Male, pubmed-meshheading:8251426-Muscle, Smooth, Vascular, pubmed-meshheading:8251426-Niacinamide, pubmed-meshheading:8251426-Nicorandil, pubmed-meshheading:8251426-Potassium Channels, pubmed-meshheading:8251426-Prostaglandin Endoperoxides, Synthetic, pubmed-meshheading:8251426-Pyridines, pubmed-meshheading:8251426-Swine, pubmed-meshheading:8251426-Vasoconstriction, pubmed-meshheading:8251426-Vasoconstrictor Agents, pubmed-meshheading:8251426-Vasodilator Agents
pubmed:year
1993
pubmed:articleTitle
Hyperpolarization induced by K+ channel openers inhibits Ca2+ influx and Ca2+ release in coronary artery.
pubmed:affiliation
Department of Pharmacology, Tohoku University School of Medicine, Sendai, Japan.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't