Linked Life Data

10709868

Source:http://linkedlifedata.com/resource/pubmed/id/10709868

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-3-29
pubmed:abstractText
Nitric oxide (NO) is generated by 3 major isoforms of nitric oxide synthase (NOS) with complex and overlapping patterns of expression. This article presents several examples of how gene targeted mice lacking endothelial and neuronal isoforms have showed various roles of NO. Neuronal NOS knockout mice are resistant to global and focal cerebral ischemia, confirming a role for neuronal NO in cellular toxicity after stroke. Endothelial NOS knockout mice have increased susceptibility to stroke consistent with a vascular protective effect of NO. They are hypertensive and lack endothelium dependent relaxing factor activity. Analysis of cardiac function shows roles for NO in suppression of inotropic responses to beta-adrenergic agonists and in mediating basal diastolic relaxation. Endothelial NOS knockout mice respond to vascular injury with increased neointimal proliferation, consistent with a physiological role for NO to suppress smooth muscle cell proliferation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0146-0005
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
87-90
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Lessons learned from nitric oxide synthase knockout animals.
pubmed:affiliation
Cardiovascular Research Center and Cardiology Division, Massachusetts General Hospital, Boston, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review