Nephrol Dial Transplant (2001) 16: 1742-1745
© 2001 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
ADMA (asymmetric dimethylarginine): an atherosclerotic disease mediating agent in patients with renal disease?
1 Department of Nephrology and 2 Institute of Clinical Pharmacology, Hannover Medical School, D-30625 Hannover, Germany
Keywords: ADMA; nitric oxide; atherosclerosis; renal disease
Introduction
Nitric oxide (NO) is a potent endogenous vasodilator that is released by endothelial cells in response to different stimuli such as shear stress. It plays a critical role in the regulation of vascular resistance and tissue blood flow. There is abundant experimental data that NO inhibits key processes of atherosclerosis, for example, monocyte adhesion, platelet aggregation, and vascular smooth muscle cell proliferation. Hence, endothelial dysfunction as a result of reduced NO activity is an early step in the course of atherosclerotic vascular disease, and evidence has accumulated that inhibition of NO synthesis by endogenous substances may be causally involved in this process [1].
Interference with NO synthesis by asymmetric dimethylarginine
NO is synthesized by stereospecific oxidation of the terminal guanidino nitrogen of the amino acid L-arginine by the action of a family of NO synthases (NOS) with endothelial, neuronal, and macrophage isoforms [2
ADMA–an innocent bystander or culprit of the atherosclerotic process?
Atherosclerosis, endothelial (dys)function and ADMA in patients with renal disease
Conclusion
Notes
References
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