Linked Life Data

12694305

Source:http://linkedlifedata.com/resource/pubmed/id/12694305

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
84
pubmed:dateCreated
2003-4-15
pubmed:abstractText
Endothelial dysfunction due to reduced availability of nitric oxide (NO) is an early step in the course of atherosclerotic vascular disease. NO is synthesized from the amino acid L-arginine by the action of the NO synthase (NOS), which can be blocked by endogenous inhibitors such as asymmetric dimethylarginine (ADMA). In laboratory animals, administration of ADMA significantly reduces NO generation, and causes an increase of blood pressure and renal vascular resistance. In clinical studies, a strong correlation between increased ADMA blood levels and impaired endothelial-dependent vasodilatation, and cardiovascular morbidity and mortality has been documented in different populations, including in patients with renal disease. Thus, ADMA seems to be the culprit, and not just an innocent biochemical bystander, of the atherosclerotic disease process. Moreover, reduced NO availability is involved in the progression of renal disease, and increased ADMA blood levels may contribute to this process. Interventions that lower ADMA blood levels in renal patients could, therefore, modulate their atherogenic profile and interfere with progression of renal failure.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0098-6577
pubmed:author
pubmed:issnType
Print
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S37-40
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Asymmetric dimethylarginine: a cardiovascular risk factor in renal disease?
pubmed:affiliation
Department of Nephrology, Hannover Medical School, Hannover, Germany. fliser.danilo@mh-hannover.de
pubmed:publicationType
Journal Article, Review