Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-5-21
pubmed:abstractText
Nitric oxide (NO) has multiple important actions that contribute to the maintenance of vascular homeostasis. NO is synthesized by three different isoforms of NO synthase (NOS), all of which have been reported to be expressed in human atherosclerotic vascular lesions. Although the regulatory roles of endothelial NOS (eNOS) and inducible NOS (iNOS) on the development of atherosclerosis have been described, little is known about the role of neuronal NOS (nNOS). Recent studies have demonstrated that nNOS also exerts important vasculoprotective effects in vivo. In a carotid artery ligation model, nNOS-knockout mice exhibited accelerated neointimal formation and constrictive vascular remodeling caused by blood flow disruption. In a rat balloon injury model, the selective inhibition of nNOS activity potently enhanced vasoconstrictor responses to a variety of calcium-mobilizing stimuli, and exacerbated neointimal formation. Moreover, in apolipoprotein E-knockout mice, deficiency of nNOS induced progression of aortic vascular lesion formation. In these models, nNOS was up-regulated in vascular lesions, and was predominantly expressed in the neointima and medial smooth muscle cells. These results provide the first direct evidence that nNOS plays important roles in suppressing arteriosclerotic vascular lesion formation. Thus, nNOS could be regarded as a novel anti-atherogenic factor.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1340-3478
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
41-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Neuronal nitric oxide synthase as a novel anti-atherogenic factor.
pubmed:affiliation
Department of Pharmacology, University of Occupational and Environmental Health, School of Medicine, 1-1 Iseigaoka, Yahatanishi-ku, Fukuoka 807-8555, Japan. mt2498@med.uoeh-u.ac.jp
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't