Linked Life Data

10666071

Source:http://linkedlifedata.com/resource/pubmed/id/10666071

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-3-2
pubmed:abstractText
Resistance arteries are an important target for vascular gene therapy because they play a key role in the regulation of tissue blood flow. The present study was designed to determine the effects of recombinant endothelial (e) nitric oxide synthase (NOS) gene expression on vasomotor reactivity of small brain stem arteries (internal diameter, 253 +/- 2.5 microm). Arterial rings were exposed ex vivo to an adenoviral vector (10(9) and 10(10) plaque-forming units/ml) encoding eNOS gene or beta-galactosidase gene. Twenty-four hours after transduction, vascular function was examined by isometric force studies. Transgene expression was evident mainly in adventitia. In arteries with endothelium transduced with eNOS gene but not with control beta-galactosidase gene, relaxations to bradykinin and substance P were significantly augmented. Removal of endothelium abolished relaxations to bradykinin and substance P in control and beta-galactosidase arteries. However, in endothelium-denuded arteries transduced with recombinant eNOS, bradykinin and substance P caused relaxations that were abolished in the presence of the NOS inhibitor N(G)-nitro-L-arginine methyl ester. In control arteries, endothelium removal augmented relaxations to the nitric oxide donors sodium nitroprusside and diethylamine NONOate. This augmentation was absent in eNOS gene-transduced arteries without endothelium. Our results suggest that, in small brain stem arteries, expression of recombinant eNOS increases biosynthesis of nitric oxide. Adventitia of small arteries is a good target for expression of recombinant eNOS. Genetically engineered adventitial cells may serve as a substitute source of nitric oxide in cerebral arteries with dysfunctional endothelium.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
278
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H420-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10666071-Animals, pubmed-meshheading:10666071-Bradykinin, pubmed-meshheading:10666071-Brain Stem, pubmed-meshheading:10666071-Cerebral Arteries, pubmed-meshheading:10666071-Dogs, pubmed-meshheading:10666071-Endothelium, Vascular, pubmed-meshheading:10666071-Enzyme Inhibitors, pubmed-meshheading:10666071-Gene Expression, pubmed-meshheading:10666071-Microcirculation, pubmed-meshheading:10666071-NG-Nitroarginine Methyl Ester, pubmed-meshheading:10666071-Nitric Oxide Donors, pubmed-meshheading:10666071-Nitric Oxide Synthase, pubmed-meshheading:10666071-Nitric Oxide Synthase Type III, pubmed-meshheading:10666071-Recombinant Proteins, pubmed-meshheading:10666071-Substance P, pubmed-meshheading:10666071-Vasoconstriction, pubmed-meshheading:10666071-Vasodilation, pubmed-meshheading:10666071-Vasomotor System
pubmed:year
2000
pubmed:articleTitle
Effects of recombinant eNOS gene expression on reactivity of small cerebral arteries.
pubmed:affiliation
Departments of Anesthesiology and Pharmacology, Mayo Clinic, Rochester, Minnesota 55905, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't