Linked Life Data

11973414

Source:http://linkedlifedata.com/resource/pubmed/id/11973414

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2002-4-25
pubmed:abstractText
Experiments were designed to study effects of raloxifene, a selective estrogen receptor modulator, on venous endothelium and smooth muscle. Rings of femoral veins with and without endothelium from adult gonadally intact, and ovariectomized female pigs were suspended for measurement of isometric force in organ chambers. Concentration-response curves to raloxifene (10-9-10-5 M) were obtained in rings at baseline tension or following contraction with prostaglandin (2 x 10-6 M) in the absence or presence of NG-monomethyl-l-arginine (l-NMMA) (nitric oxide synthase inhibitor), 1H-(1.2.4) oxadiazolo (4,3-A) quinoxalin-1-one (ODQ, soluble guanylate cyclase inhibitor), tetraethylammonium acetate (TEA; potassium channel blocker), or indomethacin (cyclooxygenase inhibitor). Raloxifene caused acute, concentration-dependent relaxations that were greater in rings with than in rings without endothelium from both groups. The l-NMMA significantly inhibited relaxations to raloxifene in rings with endothelium from ovariectomized females whereas TEA only inhibited relaxations in rings with endothelium from intact female pigs. ODQ and indomethacin significantly inhibited relaxations in rings with endothelium from both groups. These results suggest that raloxifene acutely relaxes femoral veins through release of endothelium-derived factors and by direct stimulation of vascular smooth muscle cells. Whether nitric oxide or potassium channel activation contributes to relaxations by raloxifene may depend on ovarian hormonal status of the animal.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
704-13
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11973414-Animals, pubmed-meshheading:11973414-Cyclooxygenase 1, pubmed-meshheading:11973414-Dose-Response Relationship, Drug, pubmed-meshheading:11973414-Endothelium, Vascular, pubmed-meshheading:11973414-Estrogen Antagonists, pubmed-meshheading:11973414-Estrogens, pubmed-meshheading:11973414-Female, pubmed-meshheading:11973414-Femoral Vein, pubmed-meshheading:11973414-Guanylate Cyclase, pubmed-meshheading:11973414-Indomethacin, pubmed-meshheading:11973414-Isoenzymes, pubmed-meshheading:11973414-Nitric Oxide, pubmed-meshheading:11973414-Ovariectomy, pubmed-meshheading:11973414-Ovary, pubmed-meshheading:11973414-Potassium Channel Blockers, pubmed-meshheading:11973414-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:11973414-Raloxifene, pubmed-meshheading:11973414-Receptors, Estrogen, pubmed-meshheading:11973414-Solubility, pubmed-meshheading:11973414-Swine
pubmed:year
2002
pubmed:articleTitle
Mechanism of raloxifene-induced relaxation in femoral veins depends on ovarian hormonal status.
pubmed:affiliation
Department of Physiology, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't