Relationship between G894T polymorphism (Glu 298 Asp variant) in endothelial nitric oxide synthase and nitric oxide mediated endothelial function in human atherosclerosis.

T.J. Guzik, E. Black, N.E.J. West, Denise McDonald, C. Ratnatunga, R. Pillai, K.M. Channon

Research output: Contribution to journalArticle

75 Citations (Scopus)

Abstract

Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), plays important roles in normal vascular homeostasis, and reduced endothelial NO bioactivity is an important feature of vascular disease states. The Glu298Asp (G894T) polymorphic variant of eNOS has been associated with vascular disease, but functional data are lacking. Accordingly, we examined the relationships between NO-mediated endothelial function, the presence of the eNOS Glu298Asp variant, and clinical risk factors for atherosclerosis. Endothelium-dependent vasorelaxations to different agonists were determined in human saphenous veins obtained from patients with coronary artery disease and identified risk factors (n = 104). Patients were genotyped for the eNOS G894T polymorphism. Nitric oxide-mediated endothelial vasorelaxations were highly variable between patients. Reduced vasorelaxations were associated with increased number of clinical risk factors for atherosclerosis (r = - 0.54, P
Original languageEnglish
Pages (from-to)130-137
Number of pages8
JournalAmerican Journal of Medical Genetics
Volume100(2)
Issue number2
DOIs
Publication statusPublished - 22 Mar 2001

ASJC Scopus subject areas

  • Genetics(clinical)

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