Linked Life Data

8067414

Source:http://linkedlifedata.com/resource/pubmed/id/8067414

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2 Pt 2
pubmed:dateCreated
1994-9-21
pubmed:abstractText
Isolated middle cerebral arteries of rats were perfused and superfused simultaneously with physiological salt solution (PSS) equilibrated with control (21% O2) or with reduced O2 concentrations (15, 10, 5, or 0% O2). Arterial dilation in response to reduced PO2 was unaffected by the nitric oxide synthase inhibitor N omega-nitro-L-arginine (10 microM) but was inhibited by selective perfusion of the lumen with 21% O2 PSS (0% O2 in the superfusion), endothelial removal, and 1 microM indomethacin. Arterial dilation during reduced PO2 was unaffected by 1 mM tetraethylammonium to block the Ca(2+)-dependent "maxi-K+" channel but was eliminated by 1 microM glibenclamide, a blocker of the ATP-sensitive K+ channel. Glibenclamide also inhibited dilation of the vessels in response to the stable prostacyclin analogue, iloprost. The results of this study suggest that dilation of rat middle cerebral arteries in response to reduced PO2 is mediated by an endothelium-dependent cyclooxygenase product, which activates glibenclamide-sensitive K+ channels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
267
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H580-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Role of endothelium and arterial K+ channels in mediating hypoxic dilation of middle cerebral arteries.
pubmed:affiliation
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't