Abstract
An increasing number of reports indicate that endogenously produced inhibitors of nitric oxide synthase, particularly asymmetric dimethylarginine (ADMA), regulate nitric oxide generation in disease states. This article describes the biology of ADMA and the implications for cardiovascular physiology and pathophysiology.
MeSH Terms
Amidohydrolases/antagonists & inhibitors,metabolism
Animals
Arginine/analogs & derivatives,metabolism
Cardiovascular Diseases/drug therapy,metabolism,physiopathology
Cardiovascular Physiological Phenomena
Diabetes Mellitus/metabolism
Endothelium, Vascular/metabolism,physiopathology
Enzyme Inhibitors/therapeutic use
Female
Humans
Mice
Models, Biological
Nitric Oxide/metabolism
Nitric Oxide Synthase/antagonists & inhibitors
Pre-Eclampsia/metabolism
Pregnancy
Protein-Arginine N-Methyltransferases/metabolism
Renal Insufficiency/metabolism
omega-N-Methylarginine/pharmacology
Chemicals
Enzyme Inhibitors
omega-N-Methylarginine
Nitric Oxide
N,N-dimethylarginine
Arginine
Nitric Oxide Synthase
Protein-Arginine N-Methyltransferases
Amidohydrolases
dimethylargininase
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Vallance Patrick
BHF Laboratories, Division of Medicine, University College London, Rayne Institute, 5 University St, London WC1 6JJ, UK.
[email protected]
Leiper James