Linked Life Data

10601125

Source:http://linkedlifedata.com/resource/pubmed/id/10601125

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2000-1-19
pubmed:abstractText
Epoxyeicosatrienoic acids (EETs) are cytochrome P450-derived metabolites of arachidonic acid. They are potent endogenous vasodilator compounds produced by vascular cells, and EET-induced vasodilation has been attributed to activation of vascular smooth muscle cell (SMC) K(+) channels. However, in some cells, EETs activate Ca(2+) channels, resulting in Ca(2+) influx and increased intracellular Ca(2+) concentration ([Ca(2+)](i)). We investigated whether EETs also can activate Ca(2+) channels in vascular SMC and whether the resultant Ca(2+) influx can influence vascular tone. The 4 EET regioisomers (1 micromol/L) increased porcine aortic SMC [Ca(2+)](i) by 52% to 81%, whereas arachidonic acid, dihydroxyeicosatrienoic acids, and 15-hydroxyeicosatetraenoic acid (1 micromol/L) produced little effect. The increases in [Ca(2+)](i) produced by 14,15-EET were abolished by removal of extracellular Ca(2+) and by pretreatment with verapamil (10 micromol/L), an inhibitor of voltage-dependent (L-type) Ca(2+) channels. 14,15-EET did not alter Ca(2+) signaling induced by norepinephrine and thapsigargin. When administered to porcine coronary artery rings precontracted with a thromboxane mimetic, 14,15-EET produced relaxation. However, when administered to rings precontracted with acetylcholine or KCl, 14,15-EET produced additional contractions. In rings exposed to 10 mmol/L KCl, a concentration that did not affect resting ring tension, 14,15-EET produced small contractions that were abolished by EGTA (3 mmol/L) or verapamil (10 micromol/L). These observations indicate that 14,15-EET enhances [Ca(2+)](i) influx in vascular SMC through voltage-dependent Ca(2+) channels. This 14,15-EET-induced increase in [Ca(i)(2+)] can produce vasoconstriction and therefore may act to modulate EET-induced vasorelaxation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1242-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10601125-8,11,14-Eicosatrienoic Acid, pubmed-meshheading:10601125-Animals, pubmed-meshheading:10601125-Aorta, Thoracic, pubmed-meshheading:10601125-Calcium, pubmed-meshheading:10601125-Calcium Channel Blockers, pubmed-meshheading:10601125-Cell Membrane Permeability, pubmed-meshheading:10601125-Cells, Cultured, pubmed-meshheading:10601125-Chelating Agents, pubmed-meshheading:10601125-Coronary Vessels, pubmed-meshheading:10601125-Dose-Response Relationship, Drug, pubmed-meshheading:10601125-Intracellular Fluid, pubmed-meshheading:10601125-Muscle, Smooth, Vascular, pubmed-meshheading:10601125-Muscle Contraction, pubmed-meshheading:10601125-Structure-Activity Relationship, pubmed-meshheading:10601125-Swine, pubmed-meshheading:10601125-Vasoconstrictor Agents, pubmed-meshheading:10601125-Vasodilator Agents
pubmed:year
1999
pubmed:articleTitle
Epoxyeicosatrienoic acids increase intracellular calcium concentration in vascular smooth muscle cells.
pubmed:affiliation
Department of Biochemistry, University of Iowa College of Medicine, Iowa City 52242, USA. xiang-fang@uiowa.edu
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't