Trends in Cardiovascular Medicine
Volume 16, Issue 4 , Pages 118-124, May 2006

Endothelial Dysfunction and Impaired l-arginine Transport in Hypertension and Genetically Predisposed Normotensive Subjects

  • Zhiyong Yang
  • ,
  • David M. Kaye

      Affiliations

    • Corresponding Author InformationAddress correspondence to: David M. Kaye, Baker Heart Research Institute, PO Box 6492, St Kilda Rd Central, Melbourne VIC 8008, Australia. Tel.: (+61) 3-9207-1044; fax: (+61) 3-9207-1075

Wynn Department of Metabolic Cardiology, Baker Heart Research Institute, PO Box 6492, Melbourne VIC 8008, Australia

The term endothelial dysfunction (ED) generally refers to a pathological circumstance in which normal endothelial regulation of vasomotor tone is disturbed. ED has been described in a broad range of cardiovascular and related disease states. In association, deranged endothelial function also has the potential to result in abnormal platelet aggregation and monocyte adhesion. Over the past decade, it has become apparent that reduced availability of nitric oxide is a key mechanism for ED. A range of biochemical disturbances, including depressed l-arginine, have been shown to be associated with ED, and recent evidence indicates this may be genetically determined.

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

PII: S1050-1738(06)00034-X

doi:10.1016/j.tcm.2006.02.003

Trends in Cardiovascular Medicine
Volume 16, Issue 4 , Pages 118-124, May 2006