Linked Life Data

8238579

Source:http://linkedlifedata.com/resource/pubmed/id/8238579

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5 Pt 2
pubmed:dateCreated
1993-12-20
pubmed:abstractText
Recent studies in vitro have suggested that there may be an interaction between endothelin-1 and ATP-sensitive K+ channels in vascular smooth muscle. Here we have investigated whether agents acting on membrane Ca2+ and K+ channels modulate endothelin-1-induced venoconstriction in vivo in human subjects. In a series of studies, six healthy subjects received, on separate occasions, local infusions into dorsal hand veins of endothelin-1 coinfused with 1) the ATP-sensitive K+ channel opener, cromakalim; 2) the dihydropyridine Ca2+ antagonist, nicardipine; 3) a control vasodilator, hydralazine; and 4) saline placebo. Endothelin-1 caused local venoconstriction with a maximum reduction in vein size of 66 +/- 4% at 60 min (P = 0.0001 vs. basal). Cromakalim prevented endothelin-1-induced venoconstriction (9 +/- 10% maximum constriction; P = 0.68 vs. basal). By contrast, nicardipine, in a dose sufficient to block depolarization-induced constriction caused by K+ infusion, had only a partial effect on endothelin-1-induced venoconstriction (35 +/- 8% maximum constriction; P = 0.001 vs. basal; P = 0.02 vs. endothelin-1), whereas a 10-fold higher dose of nicardipine had no additional effect and hydralazine had no effect. In further studies, cromakalim, but not nicardipine, reversed endothelin-1-induced venoconstriction. Cromakalim did not prevent constriction induced by norepinephrine. Although calcium entry through dihydropyridine-sensitive Ca2+ channels may account in part for the vasoconstrictor action of endothelin-1 in humans, the abolition of endothelin-1 responses by a K+ channel opener suggests additional mechanisms of action for endothelin-1.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
265
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1676-81
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8238579-Adult, pubmed-meshheading:8238579-Benzopyrans, pubmed-meshheading:8238579-Calcium Channels, pubmed-meshheading:8238579-Cromakalim, pubmed-meshheading:8238579-Diastole, pubmed-meshheading:8238579-Endothelins, pubmed-meshheading:8238579-Hand, pubmed-meshheading:8238579-Humans, pubmed-meshheading:8238579-Hydralazine, pubmed-meshheading:8238579-Infusions, Intravenous, pubmed-meshheading:8238579-Male, pubmed-meshheading:8238579-Muscle, Smooth, Vascular, pubmed-meshheading:8238579-Nicardipine, pubmed-meshheading:8238579-Norepinephrine, pubmed-meshheading:8238579-Potassium, pubmed-meshheading:8238579-Potassium Channels, pubmed-meshheading:8238579-Pyrroles, pubmed-meshheading:8238579-Systole, pubmed-meshheading:8238579-Time Factors, pubmed-meshheading:8238579-Vasoconstriction, pubmed-meshheading:8238579-Vasodilator Agents, pubmed-meshheading:8238579-Veins
pubmed:year
1993
pubmed:articleTitle
Venoconstriction to endothelin-1 in humans: role of calcium and potassium channels.
pubmed:affiliation
Department of Medicine, Western General Hospital, University of Edinburgh, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't